Types of action of hormones. The concept of neurohumoral relationships and hormonal regulation of functions. A Brief Overview of the Endocrine Glands

The middle lobe of the pituitary gland produces the hormone melanotropin(intermedin), which affects pigment metabolism.

The posterior lobe of the pituitary gland is closely connected with the supraoptic and paraventricular nuclei of the hypothalamus. The nerve cells of these nuclei produce neurosecretion, which is transported to the posterior lobe of the pituitary gland. Hormones accumulate in pituicytes, in these cells hormones are converted into active form. In the nerve cells of the paraventricular nucleus it is formed oxytocin, in the neurons of the supraoptic nucleus – vasopressin.

Vasopressin has two functions:

1) enhances the contraction of vascular smooth muscles (arteriole tone increases with a subsequent increase in blood pressure);

2) inhibits urine formation in the kidneys (antidiuretic effect). The antidiuretic effect is provided by the ability of vasopressin to enhance the reabsorption of water from the kidney tubules into the blood. A decrease in the formation of vasopressin is the cause of diabetes insipidus (diabetes insipidus).

Oxytocin (ocytocin) selectively acts on the smooth muscles of the uterus and enhances its contraction. The contraction of the uterus increases sharply if it was under the influence of estrogens. During pregnancy, oxytocin does not affect the contractility of the uterus, since the corpus luteum hormone progesterone makes it insensitive to all irritants. Oxytocin stimulates the release of milk; it is the excretory function that is enhanced, and not its secretion. Special cells in the mammary gland selectively respond to oxytocin. The act of sucking reflexively promotes the release of oxytocin from the neurohypophysis.

Hypothalamic regulation of pituitary hormone production

Hypothalamic neurons produce neurosecretion. Neurosecretion products that promote the formation of hormones of the anterior pituitary gland are called liberins, and those that inhibit their formation are called statins. The entry of these substances into the anterior lobe of the pituitary gland occurs through blood vessels.

Regulation of the formation of hormones of the anterior pituitary gland is carried out according to the feedback principle. There is a bilateral relationship between the tropic function of the anterior pituitary gland and the peripheral glands: tropic hormones activate peripheral endocrine glands, the latter depending on their functional state also affect the production of tropic hormones. Bilateral relationships exist between the anterior lobe of the pituitary gland and the gonads, thyroid gland and adrenal cortex. These relationships are called “plus-minus” interactions. Tropic hormones stimulate (“plus”) the function of the peripheral glands, and hormones of the peripheral glands suppress (“minus”) the production and release of hormones of the anterior pituitary gland. There is an inverse relationship between the hypothalamus and tropic hormones of the anterior pituitary gland. An increase in the concentration of pituitary hormone in the blood leads to inhibition of neurosecretion in the hypothalamus.

The sympathetic department of the autonomic nervous system enhances the production of tropic hormones, while the parasympathetic department inhibits it.

Calcitonin, or thyrocalcitonin, together with parathyroid hormone parathyroid glands participates in the regulation of calcium metabolism. Under its influence, the level of calcium in the blood decreases (hypocalcemia). This occurs as a result of the hormone’s action on bone tissue, where it activates the function of osteoblasts and enhances mineralization processes. The function of osteoclasts, which destroy bone tissue, on the contrary, is inhibited. In the kidneys and intestines, calcitonin inhibits the reabsorption of calcium and enhances the reabsorption of phosphates. The production of thyrocalcitonin is regulated by the level of calcium in the blood plasma according to the feedback type. When calcium levels decrease, the production of thyrocalcitonin is inhibited, and vice versa.

Parathyroid glands

A person has 2 pairs of parathyroid glands, located on the back surface or embedded inside the thyroid gland. The chief, or oxyphilic, cells of these glands produce parathyroid hormone, or parathyrin, or parathyroid hormone (PTH). Parathyroid hormone regulates calcium metabolism in the body and maintains its level in the blood. IN bone tissue parathyroid hormone enhances the function of osteoclasts, which leads to bone demineralization and increased calcium levels in the blood plasma (hypercalcemia). In the kidneys, parathyroid hormone enhances calcium reabsorption. In the intestine, an increase in calcium reabsorption occurs due to the stimulating effect of parathyroid hormone on the synthesis of calcitriol, an active metabolite of vitamin D3. Vitamin D3 is formed in an inactive state in the skin under the influence of ultraviolet radiation. Under the influence of parathyroid hormone, it is activated in the liver and kidneys. Calcitriol increases the formation of calcium-binding protein in the intestinal wall, which promotes the reabsorption of calcium. Influencing calcium metabolism, parathyroid hormone simultaneously affects phosphorus metabolism in the body: it inhibits the reabsorption of phosphates and increases their excretion in the urine (phosphaturia).

The activity of the parathyroid glands is determined by the calcium content in the blood plasma. If the concentration of calcium in the blood increases, this leads to a decrease in the secretion of parathyroid hormone. A decrease in calcium levels in the blood causes increased production of parathyroid hormone.

Removal of the parathyroid glands in animals or their hypofunction in humans leads to increased neuromuscular excitability, which is manifested by fibrillar twitching of single muscles, turning into spastic contractions of muscle groups, mainly the limbs, face and back of the head. The animal dies from tetanic convulsions.

Hyperfunction of the parathyroid glands leads to demineralization of bone tissue and the development of osteoporosis. Hypercalcemia increases the tendency to stone formation in the kidneys, contributes to the development of disturbances in the electrical activity of the heart, and the occurrence of ulcers in the kidneys. gastrointestinal tract as a result of increased amounts of gastrin and HCl in the stomach, the formation of which is stimulated by calcium ions.

Adrenal glands

The adrenal glands are paired glands. It is an endocrine organ that is of vital importance. The adrenal glands have two layers - the cortex and the medulla. The cortical layer is of mesodermal origin, the medulla develops from the rudiment of the sympathetic ganglion.

Adrenal cortex hormones

In the adrenal cortex there are 3 zones: the outer - glomerular, the middle - fasciculata and the inner - reticularis. The zona glomerulosa produces mainly mineralocorticoids, the zona fasciculata produces glucocorticoids, and the zona reticularis produces sex hormones (mainly androgens). According to their chemical structure, adrenal hormones are steroids. The mechanism of action of all steroid hormones is to directly influence the genetic apparatus of the cell nucleus, stimulate the synthesis of the corresponding RNA, activate the synthesis of cation transporting proteins and enzymes, and also increase the permeability of membranes to amino acids.

Mineralocorticoids.

This group includes aldosterone, deoxycorticosterone, 18-hydroxycorticosterone, 18-oxydeoxycorticosterone. These hormones are involved in the regulation of mineral metabolism. The main representative of mineralocorticoids is aldosterone. Aldosterone enhances the reabsorption of sodium and chlorine ions in the distal renal tubules and reduces the reabsorption of potassium ions. As a result, urinary sodium excretion decreases and potassium excretion increases. As sodium is reabsorbed, water reabsorption also passively increases. Due to water retention in the body, the volume of circulating blood increases, blood pressure increases, and diuresis decreases. Aldosterone has a similar effect on the exchange of sodium and potassium in the salivary and sweat glands.

Aldosterone promotes the development of the inflammatory response. Its pro-inflammatory effect is associated with increased exudation of fluid from the lumen of blood vessels into the tissue and tissue swelling. With increased production of aldosterone, the secretion of hydrogen ions and ammonium in the renal tubules also increases, which can lead to a change in the acid-base state - alkalosis.

There are several mechanisms involved in the regulation of aldosterone levels in the blood, the main one being the renin-angiotensin-aldosterone system. To a small extent, the production of aldosterone is stimulated by ACTH of the adenohypophysis. Hyponatremia or hyperkalemia stimulates the production of aldosterone through a feedback mechanism. Atrial natriuretic hormone is an aldosterone antagonist.

Glucocorticoids.

Glucocorticoid hormones include cortisol, cortisone, corticosterone, 11-deoxycortisol, 11-dehydrocorticosterone. In humans, the most important glucocorticoid is cortisol.

These hormones influence the metabolism of carbohydrates, proteins and fats:

1. Glucocorticoids cause an increase in plasma glucose (hyperglycemia). This effect is due to the stimulation of gluconeogenesis processes in the liver, i.e. the formation of glucose from amino acids and fatty acids. Glucocorticoids inhibit the activity of the hexokinase enzyme, which leads to a decrease in glucose utilization by tissues. Glucocorticoids are insulin antagonists in the regulation of carbohydrate metabolism.

2. Glucocorticoids have a catabolic effect on protein metabolism. At the same time, they also have a pronounced anti-anabolic effect, which is manifested by a decrease in synthesis especially muscle proteins, since glucocorticoids inhibit the transport of amino acids from blood plasma to muscle cells. As a result, muscle mass decreases, osteoporosis may develop, and the rate of wound healing decreases.

3. The effect of glucocorticoids on fat metabolism is to activate lipolysis, which leads to an increase in the concentration of fatty acids in the blood plasma.

4. Glucocorticoids inhibit all components of the inflammatory reaction: they reduce capillary permeability, inhibit exudation and reduce tissue swelling, stabilize lysosome membranes, which prevents the release of proteolytic enzymes that contribute to the development of the inflammatory reaction, and inhibit phagocytosis at the site of inflammation. Glucocorticoids reduce fever. This action is associated with a decrease in the release of interleukin-1 from leukocytes, which stimulates the heat production center in the hypothalamus.

5. Glucocorticoids have an antiallergic effect. This action is due to the effects underlying the anti-inflammatory effect: inhibition of the formation of factors that enhance the allergic reaction, reduction of exudation, stabilization of lysosomes. An increase in the content of glucocorticoids in the blood leads to a decrease in the number of eosinophils, the concentration of which is usually increased during allergic reactions.

6. Glucocorticoids inhibit both cellular and humoral immunity. They reduce the production of Ti B lymphocytes, reduce the formation of antibodies, and reduce immunological surveillance. With long-term use of glucocorticoids, involution of the thymus and lymphoid tissue may occur. Weakening of the body's protective immune reactions is a serious side effect of long-term treatment with glucocorticoids, as the likelihood of a secondary infection increases. In addition, the danger of developing a tumor process increases due to depression of immunological surveillance. On the other hand, these effects of glucocorticoids allow us to consider them as active immunosuppressants.

7. Glucocorticoids increase the sensitivity of vascular smooth muscle to catecholamines, which can lead to an increase in blood pressure. This is also facilitated by their slight mineralocorticoid effect: sodium and water retention in the body.

8. Glucocorticoids stimulate the secretion of hydrochloric acid.

The production of glucocorticoids by the adrenal cortex is stimulated by ACTH of the adenohypophysis. Excessive levels of glucocorticoids in the blood lead to inhibition of the synthesis of ACTH and corticoliberin by the hypothalamus. Thus, the hypothalamus, adenohypophysis and adrenal cortex are functionally united and therefore form a single hypothalamic-pituitary-adrenal system. For acute stressful situations The level of glucocorticoids in the blood quickly increases. Due to their metabolic effects, they quickly provide the body with energy material.

Hypofunction of the adrenal cortex is manifested by a decrease in the content of corticoid hormones and is called Addison's (bronze) disease. The main symptoms of this disease are: adynamia, decreased circulating blood volume, arterial hypotension, hypoglycemia, increased skin pigmentation, dizziness, vague abdominal pain, diarrhea.

With adrenal tumors, hyperfunction of the adrenal cortex with excessive production of glucocorticoids may develop. This is the so-called primary hypercorticism, or Itsenko-Cushing syndrome. Clinical manifestations of this syndrome are the same as in Itsenko-Cushing's disease.

There are five types of effects of hormones on target tissues: metabolic, morphogenetic, kinetic, corrective and reactogenic.

1. Metabolic action of hormones

Metabolic effect of hormones - causes changes in metabolism in tissues. It occurs due to three main hormonal influences.
Firstly, hormones change the permeability of cell membranes and organelles, which changes the conditions of membrane transport of substrates, enzymes, ions and metabolites and, accordingly, all types of metabolism.
Secondly, hormones change the activity of enzymes in the cell, leading to changes in their structure and configuration, facilitating connections with cofactors, reducing or increasing the intensity of the breakdown of enzyme molecules, stimulating or suppressing the activation of proenzymes.
Third, hormones change the synthesis of enzymes, inducing or suppressing their formation due to their influence on the genetic apparatus of the cell nucleus, both directly interfering with the processes of nucleic acid and protein synthesis, and indirectly through the energy and substrate-enzyme provision of these processes. Metabolic shifts caused by hormones underlie changes in cell, tissue, or organ function.

2. Morphogenetic effect hormones

Morphogenetic effect - the influence of hormones on the processes of formation, differentiation and growth of structural elements. These processes are carried out due to changes in the genetic apparatus of the cell and metabolism. Examples include the effect of growth hormone on body growth and internal organs, sex hormones - on the development of secondary sexual characteristics.

3. Kinetic action of hormones

Kinetic action is the ability of hormones to trigger the activity of an effector, to enable the implementation of a certain function. For example, oxytocin causes contraction of the muscles of the uterus, adrenaline triggers the breakdown of glycogen in the liver and the release of glucose into the blood, vasopressin turns on the reabsorption of water in the collecting ducts of the nephron, which does not occur without it.

4. Corrective action hormones

Corrective action is a change in the activity of organs or processes that occur in the absence of the hormone. An example of the corrective effect of hormones is the effect of adrenaline on heart rate, activation of oxidative processes by thyroxine, and a decrease in the reabsorption of potassium ions in the kidneys under the influence of aldosterone. A type of corrective action is the normalizing effect of hormones, when their influence is aimed at restoring an altered or even disrupted process. For example, when the anabolic processes of protein metabolism initially predominate, glucocorticoids cause a catabolic effect, but if protein breakdown initially predominates, glucocorticoids stimulate their synthesis.

In a broader sense, the dependence of the magnitude and direction of the effect of a hormone on the metabolic or functional characteristics existing before its action is determined the rule of the initial statejaniya, described at the beginning of the chapter. The initial state rule shows that hormonal effect depends not only on the number and properties of hormone molecules, but also on the reactivity of the effector, determined by the number and properties of membrane receptors for the hormone. Reactivity in this context refers to the ability of an effector to react with a certain magnitude and direction of response to the action of a specific chemical regulator.

5. Reactogenic effect of hormones

The reactogenic effect of hormones is the ability of a hormone to change the reactivity of tissue to the action of the same hormone, other hormones or mediators of nerve impulses. For example, calcium-regulating hormones reduce the sensitivity of the distal nephron to the action of vasopressin, folliculin enhances the effect of progesterone on the uterine mucosa, and thyroid hormones enhance the effects of catecholamines. A type of reactogenic action of hormones is permissive action, meaning the ability of one hormone to enable the effect of another hormone to be realized. For example, glucocorticoids have a permissive effect in relation to catecholamines, i.e. To realize the effects of adrenaline, the presence of small amounts of cortisol is necessary; insulin has a permissive effect for somatotropin (growth hormone), etc. A feature of hormonal regulation is that the reactogenic effect of hormones can be realized not only in target tissues, where the concentration of receptors for them is high, but and in other tissues and organs that have single receptors for the hormone.

The pituitary gland occupies a special position in the system of endocrine glands. It is called the central gland, since its tropic hormones regulate the activity of other endocrine glands. The pituitary gland is a complex organ; it consists of the adenohypophysis (anterior and middle lobes) and the neurohypophysis (posterior lobe). Hormones of the anterior pituitary gland are divided into two groups: growth hormone and prolactin and tropic hormones (thyrotropin, corticotropin, gonadotropin).

The first group includes somatotropin and prolactin.

Growth hormone (somatotropin) takes part in the regulation of growth, enhancing protein formation. Its most pronounced effect is on the growth of epiphyseal cartilage of the extremities; bone growth increases in length. Violation of the somatotropic function of the pituitary gland leads to various changes in the growth and development of the human body: if there is hyperfunction in childhood, then gigantism develops; with hypofunction – dwarfism. Hyperfunction in an adult does not affect overall growth, but the size of those parts of the body that are still capable of growing increases (acromegaly).

Prolactin promotes the formation of milk in the alveoli, but after preliminary exposure to female sex hormones (progesterone and estrogen). After childbirth, prolactin synthesis increases and lactation occurs. The act of sucking through a neuro-reflex mechanism stimulates the release of prolactin. Prolactin has a luteotropic effect, promotes the long-term functioning of the corpus luteum and its production of progesterone. The second group of hormones includes:

1) thyroid-stimulating hormone(thyrotropin). Selectively acts on the thyroid gland, increases its function. With reduced production of thyrotropin, atrophy of the thyroid gland occurs, with overproduction - proliferation, histological changes occur that indicate an increase in its activity;

2) adrenocorticotropic hormone (corticotropin). Stimulates production glucocorticoids adrenal glands. Corticotropin causes breakdown and inhibits protein synthesis and is a growth hormone antagonist. It inhibits the development of the basic substance connective tissue, reduces the number of mast cells, inhibits the enzyme hyaluronidase, reducing capillary permeability. This determines its anti-inflammatory effect. Under the influence of corticotropin, the size and weight of lymphoid organs decrease. The secretion of corticotropin is subject to daily fluctuations: in the evening its content is higher than in the morning;

3) gonadotropic hormones (gonadotropins - follitropin and lutropin). Present in both women and men;

a) follitropin (follicle-stimulating hormone), which stimulates the growth and development of the follicle in the ovary. It has a slight effect on the production of estrogens in women; in men, sperm formation occurs under its influence;

b) luteinizing hormone (lutropin), which stimulates the growth and ovulation of the follicle with the formation of the corpus luteum. It stimulates the formation of female sex hormones - estrogens. Lutropin promotes the production of androgens in men.

2. Hormones of the middle and posterior lobes of the pituitary gland

The middle lobe of the pituitary gland produces the hormone melanotropin(intermedin), which affects pigment metabolism.

The posterior lobe of the pituitary gland is closely connected with the supraoptic and paraventricular nuclei of the hypothalamus. The nerve cells of these nuclei produce neurosecretion, which is transported to the posterior lobe of the pituitary gland. Hormones accumulate in pituicytes; in these cells hormones are converted into an active form. In the nerve cells of the paraventricular nucleus it is formed oxytocin, in the neurons of the supraoptic nucleus – vasopressin.

Vasopressin has two functions:

1) enhances the contraction of vascular smooth muscles (arteriole tone increases with a subsequent increase in blood pressure);

Hypothalamic regulation of pituitary hormone production

Regulation of the formation of hormones of the anterior pituitary gland is carried out according to the feedback principle. There is a two-way relationship between the tropic function of the anterior pituitary gland and the peripheral glands: tropic hormones activate the peripheral endocrine glands, the latter, depending on their functional state, also affect the production of tropic hormones. Bilateral relationships exist between the anterior lobe of the pituitary gland and the gonads, thyroid gland and adrenal cortex. These relationships are called “plus-minus” interactions. Tropic hormones stimulate (“plus”) the function of the peripheral glands, and hormones of the peripheral glands suppress (“minus”) the production and release of hormones of the anterior pituitary gland. There is an inverse relationship between the hypothalamus and tropic hormones of the anterior pituitary gland. An increase in the concentration of pituitary hormone in the blood leads to inhibition of neurosecretion in the hypothalamus.

The sympathetic department of the autonomic nervous system enhances the production of tropic hormones, while the parasympathetic department inhibits it.

3. Hormones of the pineal gland, thymus, parathyroid glands

The epiphysis is located above the upper tubercles of the quadrigeminal. The meaning of the pineal gland is extremely controversial. Two compounds have been isolated from its tissue:

1) melatonin(takes part in the regulation of pigment metabolism, inhibits the development of sexual functions in young people and the action of gonadotropic hormones in adults). This is due to the direct effect of melatonin on the hypothalamus, where the release of luliberin is blocked, and on the anterior lobe of the pituitary gland, where it reduces the effect of luliberin on the release of luteropin;

2) glomerulotropin(stimulates the secretion of aldosterone by the adrenal cortex).

Thymus ( thymus) - paired lobular organ located in upper section anterior mediastinum. The thymus produces several hormones: thymosin, homeostatic thymic hormone, thymopoietin I, II, thymic humoral factor. They are playing important role in the development of immunological defense reactions of the body, stimulating the formation of antibodies. The thymus controls the development and distribution of lymphocytes. The secretion of thymic hormones is regulated by the anterior pituitary gland.

The thymus gland reaches its maximum development in childhood. After puberty, it begins to atrophy (the gland stimulates the growth of the body and inhibits the development of the reproductive system). There is an assumption that the thymus affects the exchange of Ca ions and nucleic acids.

When increasing thymus gland in children, thymic-lymphatic status occurs. In this condition, in addition to enlargement of the thymus, proliferation of lymphatic tissue occurs; enlargement of the thymus gland is a manifestation of adrenal insufficiency.

Parathyroid glands – paired organ, they are located on the surface of the thyroid gland. Parathyroid hormone – parathyroid hormone(parathyrin). Parathyroid hormone is found in gland cells in the form of a prohormone; the conversion of prohormone into parathyroid hormone occurs in the Golgi complex. From the parathyroid glands, the hormone directly enters the blood.

Parathyroid hormone regulates Ca metabolism in the body and maintains its constant level in the blood. Normally, the Ca content in the blood is 2.25-2.75 mmol/l (9-11 mg%). Skeletal bone tissue is the main depot of Ca in the body. Available certain dependence between the level of Ca in the blood and its content in bone tissue. Parathyroid hormone enhances bone resorption, which leads to an increase in the release of Ca ions, regulates the processes of deposition and release of Ca salts in the bones. Influencing Ca metabolism, parathyroid hormone simultaneously affects phosphorus metabolism: it reduces the reabsorption of phosphates in the distal tubules of the kidneys, which leads to a decrease in their concentration in the blood.

Removal of the parathyroid glands leads to lethargy, vomiting, loss of appetite, and scattered contractions. separate groups muscles that can go into prolonged tetanic contraction. Regulation of the activity of the parathyroid glands is determined by the level of Ca in the blood. If the concentration of Ca in the blood increases, this leads to a decrease in the functional activity of the parathyroid glands. As Ca levels decrease, the hormone-producing function of the glands increases.

4. Thyroid hormones. Iodinated hormones. Thyroid calcitonin. Thyroid dysfunction

Thyroid located on both sides of the trachea below the thyroid cartilage, has a lobular structure. The structural unit is a follicle filled with colloid, where the iodine-containing protein – thyroglobulin – is located.

Thyroid hormones are divided into two groups:

1) iodized – thyroxine, triiodothyronine;

2) thyrocalcitonin (calcitonin).

Iodinated hormones are formed in the follicles of glandular tissue; its formation occurs in three stages:

1) formation of colloid, synthesis of thyroglobulin;

2) iodination of the colloid, iodine entry into the body, absorption in the form of iodides. Iodides are absorbed by the thyroid gland, oxidized into elemental iodine and included in thyroglobulin, the process is stimulated by the enzyme thyroid peroxycase;

3) release into the bloodstream occurs after hydrolysis of thyroglobulin under the action of cathepsin, which releases active hormones - thyroxine, triiodothyronine.

The main active hormone of the thyroid gland is thyroxine, the ratio of thyroxine and triiodothyronine is 4: 1. Both hormones are in an inactive state in the blood; they are associated with globulin fraction proteins and blood plasma albumin. Thyroxine binds more easily to blood proteins, therefore it penetrates the cell faster and has a greater biological activity. Liver cells capture hormones; in the liver, hormones form compounds with glucuronic acid, which do not have hormonal activity and are excreted with bile in the gastrointestinal tract. This process is called detoxification, and it prevents the blood from becoming over-saturated with hormones.

The role of iodinated hormones:

1) influence on the functions of the central nervous system. Hypofunction leads to a sharp decrease in motor excitability, weakening of active and defensive reactions;

2) influence on higher nervous activity. Included in the process of developing conditioned reflexes, differentiation of inhibition processes;

3) influence on growth and development. Stimulates the growth and development of the skeleton and gonads;

4) influence on metabolism. There is an impact on the metabolism of proteins, fats, carbohydrates, and mineral metabolism. Increased energy processes and increased oxidative processes lead to increased tissue consumption of glucose, which significantly reduces fat and glycogen reserves in the liver;

5) influence on autonomic system. The number of heart contractions and breathing movements increases, sweating increases;

6) influence on the blood coagulation system. They reduce the ability of blood to clot (reduce the formation of blood clotting factors), increase its fibrinolytic activity (increase the synthesis of anticoagulants). Thyroxine inhibits the functional properties of platelets - adhesion and aggregation.

Regulation of the formation of iodine-containing hormones is carried out:

1) thyrotropin of the anterior pituitary gland. Affects all stages of iodization, the connection between hormones is carried out according to the type of direct and feedback connections;

2) iodine. Small doses stimulate the formation of the hormone by enhancing the secretion of follicles, large doses inhibit it;

3) autonomic nervous system: sympathetic - increases the activity of hormone production, parasympathetic - decreases;

4) hypothalamus. Thyrotropin-releasing hormone of the hypothalamus stimulates thyrotropin of the pituitary gland, which stimulates the production of hormones, the connection is carried out according to the type of feedback;

5) reticular formation (excitation of its structures increases the production of hormones);

6) cerebral cortex. Decortication activates the function of the gland initially, but significantly reduces it over time.

Thyrocalcitocin is formed by parafollicular cells of the thyroid gland, which are located outside the glandular follicles. It takes part in the regulation of calcium metabolism, under its influence the Ca level decreases. Thyreocalcitocin reduces phosphate levels in peripheral blood.

Thyreocalcitocin inhibits the release of Ca ions from bone tissue and increases its deposition in it. It blocks the function of osteoclasts, which destroy bone tissue, and triggers the activation mechanism of osteoblasts involved in the formation of bone tissue.

The decrease in the content of Ca and phosphate ions in the blood is due to the influence of the hormone on the excretory function of the kidneys, reducing the tubular reabsorption of these ions. The hormone stimulates the uptake of Ca ions by mitochondria.

Regulation of thyrocalcitonin secretion depends on the level of Ca ions in the blood: an increase in its concentration leads to degranulation of parafollicles. Active secretion in response to hypercalcemia maintains the concentration of Ca ions at a certain physiological level.

The secretion of thyrocalcitonin is promoted by some biologically active substances: gastrin, glucagon, cholecystokinin.

When beta-adrenergic receptors are stimulated, hormone secretion increases, and vice versa.

Thyroid gland dysfunction is accompanied by an increase or decrease in its hormone-producing function.

Insufficiency of hormone production (hypothyroidism), which appears in childhood, leads to the development of cretinism (growth is delayed, sexual development, development of the psyche, there is a violation of body proportions).

Insufficiency of hormone production leads to the development of myxedema, which is characterized by a sharp disorder of the processes of excitation and inhibition in the central nervous system, mental retardation, decreased intelligence, lethargy, drowsiness, sexual dysfunction, inhibition of all types of metabolism.

When the thyroid gland becomes overactive (hyperthyroidism), a disease occurs thyrotoxicosis. Characteristic signs: an increase in the size of the thyroid gland, the number of heartbeats, an increase in metabolism, body temperature, an increase in food consumption, bulging eyes. Increased excitability and irritability are observed, the ratio of the tone of the parts of the autonomic nervous system changes: excitation predominates sympathetic division. Muscle tremors and muscle weakness are noted.

A lack of iodine in water leads to a decrease in the function of the thyroid gland with a significant proliferation of its tissue and the formation of a goiter. Tissue proliferation is a compensatory mechanism in response to a decrease in the content of iodinated hormones in the blood.

5. Pancreatic hormones. Pancreatic dysfunction

The pancreas is a gland with mixed function. The morphological unit of the gland is the islets of Langerhans; they are mainly located in the tail of the gland. Beta cells of the islets produce insulin, alpha cells produce glucagon, and delta cells produce somatostatin. The hormones vagotonin and centropnein were found in pancreatic tissue extracts.

Insulin regulates carbohydrate metabolism, reduces blood sugar concentrations, promotes the conversion of glucose into glycogen in the liver and muscles. It increases the permeability of cell membranes to glucose: once inside the cell, glucose is absorbed. Insulin delays the breakdown of proteins and their conversion into glucose, stimulates protein synthesis from amino acids and their active transport into the cell, regulates fat metabolism through the formation of higher fatty acids from carbohydrate metabolism products, and inhibits the mobilization of fat from adipose tissue.

In beta cells, insulin is produced from its precursor proinsulin. It is transported to the cellular Golgi apparatus, where the initial stages of the conversion of proinsulin to insulin occur.

Insulin regulation is based on normal blood glucose levels: hyperglycemia leads to an increase in the flow of insulin into the blood, and vice versa.

The paraventricular nuclei of the hypothalamus increase activity during hyperglycemia, excitation goes to the medulla oblongata, from there to the pancreatic ganglia and to the beta cells, which enhances the formation of insulin and its secretion. During hypoglycemia, the hypothalamic nuclei reduce their activity and insulin secretion decreases.

Hyperglycemia directly excites the receptor apparatus of the islets of Langerhans, which increases insulin secretion. Glucose also acts directly on beta cells, leading to the release of insulin.

Glucagon increases the amount of glucose, which also leads to increased insulin production. Adrenal hormones act similarly.

Vegetative nervous system regulates insulin production through the vagus and sympathetic nerves. The vagus nerve stimulates the release of insulin, and the sympathetic nerve inhibits it.

The amount of insulin in the blood is determined by the activity of the enzyme insulinase, which destroys the hormone. Nai large quantity The enzyme is found in the liver and muscles. When blood flows through the liver once, up to 50% of the insulin in the blood is destroyed.

An important role in the regulation of insulin secretion is played by the hormone somatostatin, which is formed in the nuclei of the hypothalamus and delta cells of the pancreas. Somatostatin inhibits insulin secretion.

Insulin activity is expressed in laboratory and clinical units.

Glucagon takes part in the regulation of carbohydrate metabolism; its effect on carbohydrate metabolism is an insulin antagonist. Glucagon breaks down glycogen in the liver into glucose, and the concentration of glucose in the blood increases. Glucagon stimulates the breakdown of fats in adipose tissue.

The mechanism of action of glucagon is due to its interaction with special specific receptors that are located on the cell membrane. When glucagon binds to them, the activity of the enzyme adenylate cyclase and the concentration of cAMP increases; cAMP promotes the process of glycogenolysis.

Regulation of glucagon secretion. The formation of glucagon in alpha cells is influenced by the level of glucose in the blood. When blood glucose increases, glucagon secretion is inhibited, and when it decreases, it increases. The formation of glucagon is also influenced by the anterior lobe of the pituitary gland.

A growth hormone somatotropin increases alpha cell activity. In contrast, the delta cell hormone somatostatin inhibits the formation and secretion of glucagon, since it blocks the entry of Ca ions into alpha cells, which are necessary for the formation and secretion of glucagon.

Physiological significance lipocaine. It promotes the utilization of fats by stimulating the formation of lipids and the oxidation of fatty acids in the liver, it prevents fatty degeneration of the liver.

Functions vagotonin– increased tone of the vagus nerves, increased activity.

Functions centropnein– stimulation of the respiratory center, promoting relaxation of bronchial smooth muscles, increasing the ability of hemoglobin to bind oxygen, improving oxygen transport.

Pancreatic dysfunction.

A decrease in insulin secretion leads to the development of diabetes mellitus, the main symptoms of which are hyperglycemia, glucosuria, polyuria (up to 10 liters per day), polyphagia (increased appetite), polydyspepsia (increased thirst).

An increase in blood sugar in patients with diabetes is the result of a loss of the liver's ability to synthesize glycogen from glucose, and of cells to utilize glucose. The formation and deposition of glycogen in the muscles also slows down.

In patients with diabetes, all types of metabolism are disrupted.

6. Adrenal hormones. Glucocorticoids

The adrenal glands are paired glands located above the upper poles of the kidneys. They are of great vital importance. There are two types of hormones: cortical hormones and medulla hormones.

Cortical hormones are divided into three groups:

1) glucocorticoids (hydrocortisone, cortisone, corticosterone);

2) mineralocorticoids (aldesterone, deoxycorticosterone);

3) sex hormones (androgens, estrogens, progesterone).

Glucocorticoids are synthesized in the zona fasciculata of the adrenal cortex. According to their chemical structure, hormones are steroids; they are formed from cholesterol; ascorbic acid is required for synthesis.

Physiological significance of glucocorticoids.

Glucocorticoids affect the metabolism of carbohydrates, proteins and fats, enhance the formation of glucose from proteins, increase the deposition of glycogen in the liver, and act as insulin antagonists.

Glucocorticoids have a catabolic effect on protein metabolism, cause the breakdown of tissue protein and delay the incorporation of amino acids into proteins.

Hormones have an anti-inflammatory effect, which is due to a decrease in the permeability of the vessel walls with low activity of the enzyme hyaluronidase. The reduction in inflammation is due to inhibition of the release of arachidonic acid from phospholipids. This leads to a limitation in the synthesis of prostaglandins, which stimulate the inflammatory process.

Glucocorticoids influence the production of protective antibodies: hydrocortisone suppresses the synthesis of antibodies and inhibits the reaction between the antibody and the antigen.

Glucocorticoids have a pronounced effect on the hematopoietic organs:

1) increase the number of red blood cells by stimulating red bone marrow;

2) lead to the reverse development of the thymus gland and lymphoid tissue, which is accompanied by a decrease in the number of lymphocytes.

Excretion from the body occurs in two ways:

1) 75–90% of hormones entering the blood are removed in the urine;

2) 10–25% is removed in feces and bile.

Regulation of glucocorticoid formation.

Corticotropin of the anterior pituitary gland plays an important role in the formation of glucocorticoids. This influence is carried out on the principle of direct and feedback connections: corticotropin increases the production of glucocorticoids, and their excess content in the blood leads to inhibition of corticotropin in the pituitary gland.

Neurosecretion is synthesized in the nuclei of the anterior hypothalamus corticoliberin, which stimulates the formation of corticotropin in the anterior pituitary gland, and it, in turn, stimulates the formation of glucocorticoid. The functional relationship “hypothalamus – anterior pituitary gland – adrenal cortex” is located in a single hypothalamic-pituitary-adrenal system, which plays a leading role in the body’s adaptive reactions.

Adrenalin– hormone of the adrenal medulla – enhances the formation of glucocorticoids.

7. Adrenal hormones. Mineralocorticoids. Sex hormones

Mineralocorticoids are formed in the zona glomerulosa of the adrenal cortex and take part in the regulation of mineral metabolism. These include aldosterone And deoxycorticosterone. They enhance the reabsorption of Na ions in the renal tubules and reduce the reabsorption of K ions, which leads to an increase in Na ions in the blood and tissue fluid and an increase in them osmotic pressure. This causes water retention in the body and increases blood pressure.

Mineralocorticoids promote the manifestation inflammatory reactions by increasing capillary permeability and serous membranes. They take part in regulating the tone of blood vessels. Aldosterone has the ability to increase smooth muscle tone vascular wall, which leads to an increase in the value blood pressure. With a lack of aldosterone, hypotension develops.

Regulation of mineralocorticoid formation

Regulation of secretion and formation of aldosterone is carried out by the renin-angiotensin system. Renin is formed in special cells of the juxtaglomerular apparatus of the afferent arterioles of the kidney and is released into the blood and lymph. It catalyzes the conversion of angiotensinogen to angiotensin I, which is converted under the action of a special enzyme to angiotensin II. Angiotensin II stimulates the formation of aldosterone. The synthesis of mineralocorticoids is controlled by the concentration of Na and K ions in the blood. An increase in Na ions leads to inhibition of aldosterone secretion, which leads to the excretion of Na in the urine. A decrease in the formation of mineralocorticoids occurs when insufficient content K ions. The synthesis of mineralocorticoids is influenced by the amount of tissue fluid and blood plasma. An increase in their volume leads to inhibition of the secretion of aldosterones, which is due to the increased release of Na ions and associated water. The pineal gland hormone glomerulotropin enhances the synthesis of aldosterone.

Sex hormones (androgens, estrogens, progesterone) are formed in the reticular zone of the adrenal cortex. They have great importance in the development of the genital organs in childhood, when the intrasecretory function of the gonads is insignificant. They have an anabolic effect on protein metabolism: they increase protein synthesis due to the increased inclusion of amino acids in its molecule.

Hypofunction of the adrenal cortex causes a disease - bronze disease, or Addison's disease. Signs of this disease are: bronze coloration of the skin, especially on the arms, neck, face, increased fatigue, loss of appetite, nausea and vomiting. The patient becomes sensitive to pain and cold, and more susceptible to infection.

With hyperfunction of the adrenal cortex (the cause of which is most often a tumor), there is an increase in the formation of hormones, a predominance of the synthesis of sex hormones over others is noted, so secondary sexual characteristics begin to change dramatically in patients. In women, the manifestation of secondary male sexual characteristics is observed, in men - female ones.

8. Hormones of the adrenal medulla

The adrenal medulla produces hormones related to catecholamines. The main hormone is adrenalin, the second most important is the precursor of adrenaline - norepinephrine. Chromaffin cells of the adrenal medulla are also found in other parts of the body (on the aorta, at the site of division carotid arteries etc.), they form the adrenal system of the body. The adrenal medulla is a modified sympathetic ganglion.

The meaning of adrenaline and norepinephrine

Adrenaline performs the function of a hormone; it enters the blood constantly, when various states body (blood loss, stress, muscle activity) there is an increase in its formation and release into the blood.

Excitation of the sympathetic nervous system leads to an increase in the flow of adrenaline and norepinephrine into the blood, they prolong the effects of nerve impulses in the sympathetic nervous system. Adrenaline affects carbon metabolism, accelerates the breakdown of glycogen in the liver and muscles, relaxes bronchial muscles, inhibits gastrointestinal motility and increases the tone of its sphincters, increases the excitability and contractility of the heart muscle. It increases the tone of blood vessels, has a vasodilating effect on the vessels of the heart, lungs and brain. Adrenaline enhances the performance of skeletal muscles.

Increased activity of the adrenal system occurs under the influence of various stimuli that cause changes in the internal environment of the body. Adrenaline blocks these changes.

Adrenaline is a short-acting hormone that is quickly destroyed by monoamine oxidase. This is in full accordance with the subtle and precise central regulation of the secretion of this hormone for the development of adaptive and protective reactions of the body.

Norepinephrine functions as a mediator; it is part of sympathin, a mediator of the sympathetic nervous system; it takes part in the transmission of excitation in neurons of the central nervous system.

The secretory activity of the adrenal medulla is regulated by the hypothalamus; the higher autonomic centers of the sympathetic department are located in the posterior group of its nuclei. Their activation leads to an increase in the release of adrenaline into the blood. The release of adrenaline can occur reflexively during hypothermia, muscular work, etc. With hypoglycemia, the release of adrenaline into the blood reflexively increases.

9. Sex hormones. Menstrual cycle

The sex glands (testes in men, ovaries in women) belong to the glands with a mixed function; the intrasecretory function is manifested in the formation and secretion of sex hormones, which directly enter the blood.

Male sex hormones - androgens are formed in the interstitial cells of the testes. There are two types of androgens - testosterone And androsterone.

Androgens stimulate the growth and development of the reproductive apparatus, male sexual characteristics and the appearance of sexual reflexes.

They control the process of sperm maturation, contribute to the preservation of their motor activity, the manifestation of sexual instinct and sexual behavioral reactions, increase protein formation, especially in muscles, reduce body fat. At insufficient quantities androgen in the body disrupts inhibition processes in the cerebral cortex.

Female sex hormones estrogens are formed in the follicles of the ovary. The synthesis of estrogen is carried out by the follicle membrane, progesterone - by the corpus luteum of the ovary, which develops at the site of the burst follicle.

Estrogens stimulate the growth of the uterus, vagina, tubes, cause endometrial growth, promote the development of secondary female sexual characteristics, the manifestation of sexual reflexes, enhance the contractility of the uterus, increase its sensitivity to oxytocin, stimulate the growth and development of the mammary glands.

Progesterone ensures the process of normal pregnancy, promotes the growth of the endometrial mucosa, implantation of a fertilized egg into the endometrium, inhibits the contractility of the uterus, reduces its sensitivity to oxytocin, inhibits the maturation and ovulation of the follicle due to inhibition of the formation of pituitary lutropin.

The formation of sex hormones is influenced by the gonadotropic hormones of the pituitary gland and prolactin. In men, gonadotropic hormone promotes the maturation of sperm, in women – the growth and development of the follicle. Lutropin determines the production of female and male sex hormones, ovulation and the formation of the corpus luteum. Prolactin stimulates the production of progesterone.

Melatonin inhibits the activity of the gonads.

The nervous system takes part in the regulation of the activity of the gonads due to the formation of gonadotropic hormones in the pituitary gland. The central nervous system regulates the course of sexual intercourse. When the functional state of the central nervous system changes, disruption of the sexual cycle and even its cessation may occur.

Menstrual cycle includes four periods.

1. Pre-ovulation (from the fifth to the fourteenth day). The changes are caused by the action of follitropin, increased formation of estrogens occurs in the ovaries, they stimulate the growth of the uterus, the proliferation of the mucous membrane and its glands, the maturation of the follicle accelerates, its surface ruptures, and an egg is released from it - ovulation occurs.

2. Ovulation (from the fifteenth to the twenty-eighth day). It begins with the release of the egg into the tube, contraction of the smooth muscles of the tube helps propel it towards the uterus, where fertilization can occur. A fertilized egg, entering the uterus, attaches to its mucous membrane and pregnancy occurs. If fertilization does not occur, the post-ovulation period begins. The corpus luteum develops at the site of the follicle and produces progesterone.

3. Post-ovulation period. An unfertilized egg dies when it reaches the uterus. Progesterone reduces the formation of follitropin and reduces the production of estrogen. The changes that have occurred in the woman’s genitals disappear. At the same time, the formation of lutropin decreases, which leads to atrophy of the corpus luteum. Due to the decrease in estrogen, the uterus contracts and the mucous membrane is rejected. Subsequently, its regeneration occurs.

4. The rest period and post-ovulation period last from the first to the fifth day of the sexual cycle.

10. Hormones of the placenta. The concept of tissue hormones and antihormones

The placenta is a unique formation that connects the maternal body with the fetus. It performs numerous functions, including metabolic and hormonal. It synthesizes hormones of two groups:

1) protein – human chorionic gonadotropin (CG), placental lactogenic hormone (PLG), relaxin;

2) steroids – progesterone, estrogens.

HCG is formed in large quantities after 7-12 weeks of pregnancy; subsequently, the formation of the hormone decreases several times, its secretion is not controlled by the pituitary gland and hypothalamus, and its transport to the fetus is limited. The functions of hCG are to increase the growth of follicles, the formation of the corpus luteum, and stimulate the production of progesterone. The protective function is the ability to prevent rejection of the embryo by the mother's body. HCG has an antiallergic effect.

PLG begins to be secreted from the sixth week of pregnancy and increases progressively. It affects the mammary glands, like pituitary prolactin, on protein metabolism (increases protein synthesis in the mother’s body). At the same time, the content of free fatty acids increases and insulin resistance increases.

Relaxin is secreted in the later stages of pregnancy, relaxes the ligaments of the symphysis pubis, reduces the tone of the uterus and its contractility.

Progesterone is synthesized by the corpus luteum until the fourth to sixth week of pregnancy; subsequently, the placenta is involved in this process, and the secretion process progressively increases. Progesterone causes relaxation of the uterus, a decrease in its contractility and sensitivity to estrogens and oxytocin, accumulation of water and electrolytes, especially intracellular sodium. Estrogens and progesterone promote growth, uterine distension, mammary gland development and lactation.

Tissue hormones are biologically active substances that act at the site of their formation and do not enter the blood. Prostaglandins are formed in microsomes of all tissues, take part in the regulation of the secretion of digestive juices, changes in the tone of smooth muscles of blood vessels and bronchi, and the process of platelet aggregation. Tissue hormones that regulate local blood circulation include histamine(dilates blood vessels) and serotonin(has a pressor effect). Tissue hormones are considered to be mediators of the nervous system - norepinephrine and acetylcholine.

Antihormones– substances with antihormonal activity. Their formation occurs during prolonged administration of the hormone into the body from the outside. Each antihormone has a pronounced species specificity and blocks the action of the type of hormone for which it was produced. It appears in the blood 1–3 months after the administration of the hormone and disappears 3–9 months after the last injection of the hormone.

Internal secretion (incretion) is the secretion of specialized biologically active substances - hormones- into the internal environment of the body (blood or lymph). Term "hormone" was first applied to secretin (the gut hormone) by Starling and Baylis in 1902. Hormones differ from other biologically active substances, for example, metabolites and mediators, in that they, firstly, are formed by highly specialized endocrine cells, and secondly, in that they influence tissues distant from the gland through the internal environment, i.e. have a distant effect.

The most ancient form of regulation is humoral-metabolic(diffusion of active substances to neighboring cells). She in various forms occurs in all animals, especially clearly manifested in embryonic period. The nervous system, as it developed, subordinated itself to humoral-metabolic regulation.

True endocrine glands appeared late, but in the early stages of evolution there are neurosecretion. Neurosecrets are not mediators. Mediators are simpler compounds, work locally in the synapse area and are quickly destroyed, while neurosecrets are protein substances, break down more slowly and work over a long distance.

With the advent circulatory system neurosecrets began to be released into her cavity. Then special formations arose to accumulate and change these secretions (in ringed fish), then their appearance became more complex and the epithelial cells themselves began to release their secretions into the blood.

Endocrine organs have a variety of origins. Some of them arose from the sense organs (the pineal gland - from the third eye). Other endocrine glands were formed from the exocrine glands (thyroid). Branchiogenic glands were formed from the remains of provisional organs (thymus, parathyroid glands). Steroid glands originate from the mesoderm, from the walls of the coelom. Sex hormones are secreted by the walls of glands containing germ cells. Thus, different endocrine organs have different origins, but they all arose as an additional mode of regulation. There is a unified neurohumoral regulation in which the nervous system plays a leading role.

Why was such an addition to nervous regulation formed? Neural communication is fast, precise, and locally addressed. Hormones act more widely, more slowly, longer. They provide a long-term reaction without the participation of the nervous system, without constant impulses, which is uneconomical. Hormones have a long aftereffect. When required fast reaction- the nervous system works. When a slower and more sustained response to slow and lasting changes environment - hormones work (spring, autumn, etc.), providing all adaptive changes in the body, including sexual behavior. In insects, hormones completely ensure all metamorphosis.

The nervous system acts on the glands in the following ways:

1. Through neurosecretory fibers of the autonomic nervous system;

2.Through neurosecrets - the formation of the so-called. releasing or inhibiting factors;

3. The nervous system can change the sensitivity of tissues to hormones.

Hormones also affect the nervous system. There are receptors that respond to ACTH, to estrogens (in the uterus), hormones affect the GNI (sexual), the activity of the reticular formation and hypothalamus, etc. Hormones influence behavior, motivation and reflexes, and are involved in stress reactions.

There are reflexes in which the hormonal part is included as a link. For example: cold - receptor - central nervous system - hypothalamus - releasing factor - secretion of thyroid-stimulating hormone - thyroxine - increase in cellular metabolism - increase in body temperature.

Neurosecretion. Neurosecretion is the ability of specialized nerve cells synthesize and release peptides into the blood and cerebrospinal fluid, called neurohormones. This function is primarily possessed by hypothalamic neurons. The neurosecretion formed in the cell soma is stored in the form of granules and, through axonal transport, is transported either for storage in the posterior lobe of the pituitary gland (vasopressin and oxytocin), or through axovasal contacts it enters the capillaries of the portal vein of the pituitary gland and is transported through the bloodstream to the adenohypophysis or enters the cerebrospinal fluid (vasopressin, oxytocin, neurotensin, etc.), or are transferred to other parts of the brain, where peptides released on axons act as mediators or modulators of nervous processes.

All peptide neurohormones, depending on their biological effects and target organs, are divided into 3 groups:

1. Viscero-receptive neurohormones that have a predominant effect on visceral organs(vasopressin, oxytocin).

2. Neuroreceptive neurohormones or neuromodulators that have pronounced effects on the functions of the nervous system and have analgesic, sedative, cataleptic, motivational, behavioral and emotional effects, effects on memory and thinking (endorphins, enkephalins, neurotensin, vasopressin, etc.).

3. Adenohypophysiotropic neurohormones that regulate the activity of glandular cells of the adenohypophysis ((stimulators of pituitary hormones - liberins and inhibitors - statins).

The central nervous system has two ways of controlling endocrine organs - direct (cerebroglandular) and indirect (cerebro-pituitary (Pituitarium - pituitary gland)). Both of these pathways are widely used in the body.

Types of hormonal effects.

Hormones have a fairly wide range of effects on the cells, organs and tissues of the body.

1.Metabolic effect.. The influence of hormones on metabolism is carried out by changing the permeability of the membrane for substrates and coenzymes, by changing the quantity, activity and affinity of enzymes, through the influence on the genetic apparatus.

2.Morphogenetic effect. The influence of hormones on the processes of cell formation, differentiation and growth, metamorphosis. It is carried out by changing the genetic apparatus of cells and metabolism, including the intake, absorption, transport and disposal of plastic substances. Examples include the effect of somatotropin on body growth, sex hormones on development

secondary sexual characteristics, etc.

3.Kinetic effect. The action of hormones, triggering the activity of the effector, including the work certain type activities. For example, oxytocin causes contraction of the uterine muscles, thyrotropin causes the synthesis and secretion of thyroid hormones, adrenaline causes the breakdown of glycogen and the release of glucose into the blood.

4. Corrective effect. The action of hormones that changes the activity of organs or processes that occur in the absence of the hormone. A type of corrective effect is the normalizing effect of hormones, when their influence is aimed at restoring an altered or disrupted process. An example of a corrective effect is the effect of adrenaline on heart rate, activation of oxidative processes by thyroxine, and reduction of potassium ion reabsorption by aldosterone.

5.Permissive effect. The effect of hormones on the effector, allowing the influence of other regulators, including hormones, to manifest themselves. For example, the presence of glucocorticoids is necessary for the implementation of the vasoconstrictor effect of the sympathetic nervous system, insulin and glucocorticoids are necessary for the implementation of the metabolic effect of somatotropin.

Hormonal function of the adenohypophysis.

The cells of the adenohypophysis (see their structure and composition in the histology course) produce the following hormones: somatotropin (growth hormone), prolactin, thyrotropin (thyroid-stimulating hormone), follicle-stimulating hormone, luteinizing hormone, corticotropin (ACTH), melanotropin, beta-endorphin, diabetogenic peptide, exophthalmic factor and ovarian growth hormone. Let's take a closer look at the effects of some of them.

Corticotropin . (adrenocorticotropic hormone - ACTH) is secreted by the adenohypophysis in continuously pulsating bursts that have a clear daily rhythm. The secretion of corticotropin is regulated by direct and feedback connections. The direct connection is represented by the hypothalamic peptide - corticoliberin, which enhances the synthesis and secretion of corticotropin. Feedback is triggered by the content of cortisol in the blood (a hormone of the adrenal cortex) and is closed both at the level of the hypothalamus and the adenohypophysis, and an increase in the concentration of cortisol inhibits the secretion of corticotropin and corticotropin.

Corticotropin has two types of action - adrenal and extra-adrenal. The adrenal action is the main one and consists of stimulating the secretion of glucocorticoids, and to a much lesser extent, mineralocorticoids and androgens. The hormone enhances the synthesis of hormones in the adrenal cortex - steroidogenesis and protein synthesis, leading to hypertrophy and hyperplasia of the adrenal cortex. The extra-adrenal effect is lipolysis of adipose tissue, increased insulin secretion, hypoglycemia, increased deposition melanin with hyperpigmentation.

Excess corticotropin is accompanied by the development of hypercortisolism with a predominant increase in cortisol secretion and is called “Itsenko-Cushing’s disease.” The main manifestations are typical for excess glucocorticoids: obesity and other metabolic changes, a decrease in the effectiveness of immune mechanisms, development arterial hypertension and the possibility of diabetes. Corticotropin deficiency causes insufficiency of glucocorticoid function of the adrenal glands with pronounced metabolic changes, as well as a decrease in the body's resistance to unfavorable environmental conditions.

Somatotropin. . Growth hormone has a wide range of metabolic effects that provide morphogenetic effects. The hormone affects protein metabolism, enhancing anabolic processes. It stimulates the supply of amino acids into cells, protein synthesis by accelerating translation and activating RNA synthesis, increases cell division and tissue growth, and inhibits proteolytic enzymes. Stimulates the incorporation of sulfate into cartilage, thymidine into DNA, proline into collagen, uridine into RNA. The hormone causes a positive nitrogen balance. Stimulates the growth of epiphyseal cartilage and their replacement with bone tissue by activating alkaline phosphatase.

The effect on carbohydrate metabolism is twofold. On the one hand, somatotropin increases insulin production both due to a direct effect on beta cells and due to the hormone-induced hyperglycemia caused by the breakdown of glycogen in the liver and muscles. Somatotropin activates liver insulinase, an enzyme that destroys insulin. On the other hand, somatotropin has a contrainsular effect, inhibiting the utilization of glucose in tissues. This combination of effects, in the presence of a predisposition in conditions of excessive secretion, can cause diabetes mellitus, called pituitary in origin.

The effect on fat metabolism is to stimulate lipolysis of adipose tissue and the lipolytic effect of catecholamines, increasing the level of free fatty acids in the blood; due to their excessive intake into the liver and oxidation, the formation of ketone bodies increases. These effects of somatotropin are also classified as diabetogenic.

If an excess of the hormone occurs in early age, gigantism is formed with proportional development of the limbs and torso. An excess of the hormone in adolescence and adulthood causes increased growth of the epiphyseal areas of skeletal bones, areas with incomplete ossification, which is called acromegaly. . Internal organs also increase in size - splanchomegaly.

At congenital deficiency hormone, dwarfism is formed, called “pituitary dwarfism”. After the publication of J. Swift's novel about Gulliver, such people are called colloquial speech Lilliputians. In other cases, acquired hormone deficiency causes mild growth retardation.

Prolactin . The secretion of prolactin is regulated by hypothalamic peptides - the inhibitor prolactinostatin and the stimulator prolactoliberin. The production of hypothalamic neuropeptides is under dopaminergic control. The level of estrogen and glucocorticoids in the blood affects the amount of prolactin secretion

and thyroid hormones.

Prolactin specifically stimulates mammary gland development and lactation, but not its secretion, which is stimulated by oxytocin.

In addition to the mammary glands, prolactin affects the sex glands, helping to maintain the secretory activity of the corpus luteum and the formation of progesterone. Prolactin is a regulator of water-salt metabolism, reducing the excretion of water and electrolytes, potentiates the effects of vasopressin and aldosterone, stimulates the growth of internal organs, erythropoiesis, and promotes the manifestation of the maternal instinct. In addition to enhancing protein synthesis, it increases the formation of fat from carbohydrates, contributing to postpartum obesity.

Melanotropin . . It is formed in the cells of the intermediate lobe of the pituitary gland. Melanotropin production is regulated by hypothalamic melanoliberin. The main effect of the hormone is on the melanocytes of the skin, where it causes depression of pigment in the processes, an increase in free pigment in the epidermis surrounding the melanocytes, and an increase in melanin synthesis. Increases pigmentation of skin and hair.

Vasopressin . . It is formed in the cells of the supraoptic and paraventricular nuclei of the hypothalamus and accumulates in the neurohypophysis. The main stimuli that regulate the synthesis of vasopressin in the hypothalamus and its secretion into the blood by the pituitary gland can generally be called osmotic. They are represented by: a) an increase in the osmotic pressure of the blood plasma and stimulation of vascular osmoreceptors and osmoreceptor neurons of the hypothalamus; b) an increase in sodium content in the blood and stimulation of hypothalamic neurons that act as sodium receptors; c) a decrease in the central volume of circulating blood and blood pressure, perceived by volume receptors of the heart and mechanoreceptors of blood vessels;

d) emotional pain stress and physical activity; e) activation of the renin-angiotensin system and the effect of angiotensin stimulating neurosecretory neurons.

The effects of vasopressin are realized due to the binding of the hormone in tissues to two types of receptors. Binding to Y1-type receptors, predominantly localized in the wall of blood vessels, through the second messengers inositol triphosphate and calcium causes vascular spasm, which contributes to the name of the hormone - “vasopressin”. Binding to Y2-type receptors in the distal parts of the nephron through the secondary messenger c-AMP ensures an increase in the permeability of the nephron collecting ducts to water, its reabsorption and urine concentration, which corresponds to the second name of vasopressin - “antidiuretic hormone, ADH”.

In addition to its effect on the kidney and blood vessels, vasopressin is one of the important brain neuropeptides involved in the formation of thirst and drinking behavior, memory mechanisms, and regulation of the secretion of adenopituitary hormones.

Lack or even complete absence Vasopressin secretion manifests itself in the form of a sharp increase in diuresis with the release of large amounts of hypotonic urine. This syndrome is called " diabetes insipidus", it can be congenital or acquired. Excess vasopressin syndrome (Parhon syndrome) manifests itself

in excessive fluid retention in the body.

Oxytocin . The synthesis of oxytocin in the paraventricular nuclei of the hypothalamus and its release into the blood from the neurohypophysis is stimulated by a reflex pathway when irritating the stretch receptors of the cervix and the receptors of the mammary glands. Estrogens increase the secretion of oxytocin.

Oxytocin causes the following effects: a) stimulates contraction of the smooth muscles of the uterus, promoting childbirth; b) causes contraction of smooth muscle cells of the excretory ducts of the lactating mammary gland, ensuring the release of milk; c) has a diuretic and natriuretic effect under certain conditions; d) participates in the organization of drinking and eating behavior; e) is an additional factor in the regulation of the secretion of adenopituitary hormones.

Hormonal function of the adrenal glands .

Mineralocorticoids are secreted in the zona glomerulosa of the adrenal cortex. The main mineralocorticoid is aldosterone .. This hormone is involved in the regulation of the exchange of salts and water between internal and external environment, predominantly affecting the tubular apparatus of the kidneys, as well as the sweat and salivary glands, and the intestinal mucosa. Acting on the cell membranes of the vascular network and tissues, the hormone also provides regulation of the exchange of sodium, potassium and water between the extracellular and intracellular environment.

The main effects of aldosterone in the kidneys are increased sodium reabsorption in the distal tubules with its retention in the body and increased urinary potassium excretion with a decrease in the cation content in the body. Under the influence of aldosterone, the body retains chlorides, water, and increases the excretion of hydrogen ions, ammonium, calcium and magnesium. The volume of circulating blood increases, a shift in acid-base balance towards alkalosis is formed. Aldosterone can have a glucocorticoid effect, but it is 3 times weaker than cortisol and physiological conditions does not appear.

Mineralocorticoids are vital important hormones, since the death of the body after removal of the adrenal glands can be prevented by introducing hormones from the outside. Mineralocorticoids increase inflammation, which is why they are sometimes called anti-inflammatory hormones.

The main regulator of the formation and secretion of aldosterone is angiotensin II, which made it possible to consider aldosterone part renin-angiotensin-aldosterone system (RAAS), providing regulation of water-salt and hemodynamic homeostasis. The feedback link in the regulation of aldosterone secretion is realized by changing the level of potassium and sodium in the blood, as well as the volume of blood and extracellular fluid, and the sodium content in the urine of the distal tubules.

Excessive production of aldosterone - aldosteronism - can be primary or secondary. In primary aldosteronism, the adrenal gland, due to hyperplasia or tumor of the zona glomerulosa (Cohn syndrome), produces increased quantities hormone, which leads to sodium and water retention in the body, edema and arterial hypertension, loss of potassium and hydrogen ions through the kidneys, alkalosis and shifts in the excitability of the myocardium and nervous system. Secondary aldosteronism is the result of excess production of angiotensin II and increased stimulation of the adrenal glands.

Aldosterone deficiency due to adrenal damage pathological process It is rarely isolated and is often combined with a deficiency of other cortical hormones. Leading violations are noted from the outside cardiovascular and nervous systems, which is associated with inhibition of excitability,

a decrease in BCC and changes in electrolyte balance.

Glucocorticoids (cortisol and corticosterone) influence all types of exchange.

Hormones have mainly catabolic and antianabolic effects on protein metabolism and cause a negative nitrogen balance. protein breakdown occurs in muscle and connective bone tissue, and the level of albumin in the blood drops. The permeability of cell membranes to amino acids decreases.

The effects of cortisol on fat metabolism are due to a combination of direct and indirect effects. The synthesis of fat from carbohydrates is suppressed by cortisol itself, but due to hyperglycemia caused by glucocorticoids and increased insulin secretion, fat formation increases. Fat is deposited in

upper body, neck and face.

The effects on carbohydrate metabolism are generally opposite to that of insulin, which is why glucocorticoids are called contrainsular hormones. Under the influence of cortisol, hyperglycemia occurs due to: 1) increased formation of carbohydrates from amino acids through gluconeogenesis; 2) suppression of glucose utilization by tissues. The consequence of hyperglycemia is glycosuria and stimulation of insulin secretion. A decrease in cell sensitivity to insulin, combined with contrainsular and catabolic effects, can lead to the development of steroid-induced diabetes mellitus.

The systemic effects of cortisol manifest themselves in the form of a decrease in the number of lymphocytes, eosinophils and basophils in the blood, an increase in neutrophils and red blood cells, an increase in sensory sensitivity and excitability of the nervous system, an increase in the sensitivity of adrenergic receptors to the action of catecholamines, maintaining an optimal functional state and regulating the cardiovascular system. vascular system. Glucocorticoids increase the body's resistance to excessive irritants and suppress inflammation and allergic reactions, which is why they are called adaptive and anti-inflammatory hormones.

Excess glucocorticoids not associated with increased secretion of corticotropin is called Itsenko-Cushing syndrome. Its main manifestations are similar to Itsenko-Cushing's disease, however, thanks to feedback, the secretion of corticotropin and its level in the blood are significantly reduced. Muscle weakness, a tendency to diabetes mellitus, hypertension and sexual dysfunction, lymphopenia, peptic ulcers of the stomach, mental changes - this is not a complete list of symptoms of hypercortisolism.

Glucocorticoid deficiency causes hypoglycemia, decreased body resistance, neutropenia, eosinophilia and lymphocytosis, impaired adrenoreactivity and cardiac activity, and hypotension.

Catecholamines - hormones of the adrenal medulla, represented by adrenaline and norepinephrine , which are secreted in a 6:1 ratio.

Main metabolic effects. adrenaline are: increased breakdown of glycogen in the liver and muscles (glycogenolysis) due to activation of phosphorylase, suppression of glycogen synthesis, suppression of glucose consumption by tissues, hyperglycemia, increased oxygen consumption by tissues and oxidative processes in them, activation of the breakdown and mobilization of fat and its oxidation.

Functional effects of catecholamines. depend on the predominance of one of the types of adrenergic receptors (alpha or beta) in the tissues. For adrenaline, the main functional effects are manifested in the form of: increased frequency and intensification of heart contractions, improved conduction of excitation in the heart, constriction of blood vessels in the skin and organs abdominal cavity; increasing heat generation in tissues, weakening contractions of the stomach and intestines, relaxing bronchial muscles, dilating pupils, reducing glomerular filtration and urine formation, stimulation of renin secretion by the kidney. Thus, adrenaline improves the body’s interaction with the external environment and increases performance in emergency conditions. Adrenaline is a hormone of urgent (emergency) adaptation.

The release of catecholamines is regulated by the nervous system through sympathetic fibers passing through the splanchnic nerve. Nerve centers that regulate secretory function chromaffin tissue, located in the hypothalamus.

Thyroid hormonal function.

Thyroid hormones are triiodothyronine and tetraiodothyronine (thyroxine ). The main regulator of their secretion is the adenohypophysis hormone thyrotropin. In addition, there is direct nervous regulation of the thyroid gland through the sympathetic nerves. Feedback is carried out by the level of hormones in the blood and is closed in both the hypothalamus and the pituitary gland. The intensity of secretion of thyroid hormones affects the volume of their synthesis in the gland itself (local feedback).

Main metabolic effects. thyroid hormones are: increasing the absorption of oxygen by cells and mitochondria, activation of oxidative processes and increasing basal metabolism, stimulation of protein synthesis by increasing the permeability of cell membranes for amino acids and activation of the genetic apparatus of the cell, lipolytic effect, activation of the synthesis and excretion of cholesterol with bile, activation of glycogen breakdown , hyperglycemia, increased tissue glucose consumption, increased glucose absorption in the intestine, activation of liver insulinase and acceleration of insulin inactivation, stimulation of insulin secretion due to hyperglycemia.

The main functional effects of thyroid hormones are: ensuring normal processes of growth, development and differentiation of tissues and organs, activation of sympathetic effects by reducing the breakdown of the mediator, the formation of catecholamine-like metabolites and increasing the sensitivity of adrenergic receptors (tachycardia, sweating, vasospasm, etc.), increasing heat generation and body temperature, activation of the internal nervous system and increased excitability of the central nervous system, increased energy efficiency mitochondria and myocardial contractility, a protective effect against the development of myocardial damage and ulcer formation in the stomach under stress, an increase in renal blood flow, glomerular filtration and diuresis, stimulation of regeneration and healing processes, ensuring normal reproductive activity.

Increased secretion of thyroid hormones is a manifestation of hyperfunction of the thyroid gland - hyperthyroidism. At the same time, it is noted characteristic changes metabolism (increased basal metabolism, hyperglycemia, weight loss, etc.), symptoms of excessive sympathetic effects (tachycardia, increased sweating, increased excitability, increased blood pressure, etc.). Maybe

develop diabetes.

Congenital deficiency of thyroid hormones impairs the growth, development and differentiation of the skeleton, tissues and organs, including the nervous system (mental retardation occurs). This congenital pathology called "cretinism". Acquired thyroid deficiency or hypothyroidism manifests itself in a slowdown of oxidative processes, a decrease in basal metabolism, hypoglycemia, degeneration of subcutaneous fat and skin with the accumulation of glycosaminoglycans and water. The excitability of the central nervous system decreases, weakens sympathetic effects and heat production. The complex of such disorders is called “myxedema”, i.e. mucous swelling.

Calcitonin - Produced in parafollicular K cells of the thyroid gland. The target organs for calcitonin are bones, kidneys and intestines. Calcitonin reduces calcium levels in the blood by facilitating mineralization and inhibiting bone resorption. Reduces the reabsorption of calcium and phosphate in the kidneys. Calcitonin inhibits the secretion of gastrin in the stomach and reduces acidity gastric juice. The secretion of calcitonin is stimulated by an increase in the level of Ca++ in the blood and gastrin.

Hormonal functions of the pancreas .

Sugar-regulating hormones, i.e. Many hormones of the endocrine glands influence blood sugar and carbohydrate metabolism. But the most pronounced and powerful effects are exerted by the hormones of the islets of Langerhans of the pancreas - insulin and glucagon . The first of them can be called hypoglycemic, as it reduces blood sugar levels, and the second - hyperglycemic.

Insulin has a powerful effect on all types of metabolism. Its effect on carbohydrate metabolism is mainly manifested by the following effects: it increases the permeability of cell membranes in muscles and adipose tissue for glucose, activates and increases the content of enzymes in cells, enhances the utilization of glucose by cells, activates phosphorylation processes, suppresses the breakdown and stimulates the synthesis of glycogen, inhibits gluconeogenesis , activates glycolysis.

The main effects of insulin on protein metabolism: increasing membrane permeability for amino acids, enhancing the synthesis of proteins necessary for the formation

nucleic acids, primarily mRNA, activation of amino acid synthesis in the liver, activation of synthesis and suppression of protein breakdown.

The main effects of insulin on fat metabolism: stimulation of the synthesis of free fatty acids from glucose, stimulation of triglyceride synthesis, suppression of fat breakdown, activation of ketone body oxidation in the liver.

Glucagon causes the following main effects: activates glycogenolysis in the liver and muscles, causes hyperglycemia, activates gluconeogenesis, lipolysis and suppression of fat synthesis, increases the synthesis of ketone bodies in the liver, stimulates protein catabolism in the liver, increases urea synthesis.

The main regulator of insulin secretion is D-glucose in the incoming blood, which activates a specific pool of cAMP in beta cells and, through this intermediary, leads to stimulation of the release of insulin from secretory granules. The intestinal hormone gastric inhibitory peptide (GIP) enhances the response of beta cells to the action of glucose. Through a nonspecific, glucose-independent pool, cAMP stimulates insulin secretion and CA++ ions. The nervous system also plays a certain role in the regulation of insulin secretion, in particular nervus vagus and acetylcholine stimulate insulin secretion, and sympathetic nerves and catecholamines through alpha-adrenergic receptors suppress insulin secretion and stimulate glucagon secretion.

A specific inhibitor of insulin production is the hormone of delta cells of the islets of Langerhans - somatostatin . This hormone is also formed in the intestines, where it inhibits the absorption of glucose and thereby reduces the response of beta cells to a glucose stimulus.

Glucagon secretion is stimulated by a decrease in blood glucose levels, under the influence of gastrointestinal hormones (GIP, gastrin, secretin, pancreozymin-cholecystokinin) and by a decrease in the content of CA++ ions, and is inhibited by insulin, somatostatin, glucose and calcium.

Absolute or relative deficiency of insulin in relation to glucagon manifests itself in the form of diabetes mellitus. With this disease, profound metabolic disorders occur and, if insulin activity is not restored artificially from the outside, death may occur. Diabetes mellitus is characterized by hypoglycemia, glucosuria, polyuria, thirst, constant feeling hunger, ketonemia, acidosis, weakness of the immune system, circulatory failure and many other disorders. An extremely severe manifestation of diabetes mellitus is diabetic coma.

Parathyroid glands.

The parathyroid glands secrete parathyroid hormone n, which, acting on three main target organs (bones, kidney and intestines), through cAMP causes hypercalcemia, hyperphosphatemia and hyperphosphaturia. The effect of parathyroid hormone on bone tissue is due to the stimulation and increase in the number of osteoclasts that resorb bone, as well as the formation of excess citric and lactic acids, which acidify the environment. This slows down activity alkaline phosphatase- an enzyme necessary for the formation of the main bone mineral - calcium phosphate. Excess citric and lactic acids lead to the formation of soluble calcium salts, leaching them into the blood and demineralization of bone tissue.

In the kidneys, parathyroid hormone reduces the reabsorption of calcium in the proximal tubules, but strongly stimulates the reabsorption of calcium in the distal tubules, which prevents calcium loss in the urine. Phosphate reabsorption is inhibited in both the proximal and distal nephron, causing phosphaturia. In addition, parathyroid hormone causes diuretic and natriuretic effects.

In the intestine, parathyroid hormone activates calcium absorption. In many other tissues, parathyroid hormone stimulates the entry of calcium into the blood, the transport of Ca++ from the cytosol to intracellular stores and its removal from the cell. In addition, parathyroid hormone stimulates the secretion of acid and pepsin in the stomach.

The main regulator of parathyroid hormone secretion is the level of ionized calcium (Ca++) in the extracellular environment. A low concentration of calcium stimulates the secretion of the hormone, which is associated with an increase in the content of cAMP in the cells of the parathyroid glands. Therefore, they stimulate the secretion of parathyroid hormone and catecholamines through beta adrenergic receptors. Suppress secretion by high levels of Ca++ and calcitrio l(active metabolite of vitamin D).

Increased secretion of parathyroid hormone in hyperplasia or adenoma of the parathyroid glands is accompanied by demineralization of the skeleton and deformation of the long tubular bones, decreased bone density on x-ray, formation of kidney stones, muscle weakness, depression, memory and concentration problems.

Hormonal function of the pineal gland.

In the pineal gland ( pineal gland) is formed melatonin , which is a derivative of tryptophan. Melatonin synthesis depends on lighting, because excess light inhibits its formation. The direct stimulator-mediator of the synthesis and secretion of melatonin is norepinephrine, released by sympathetic nerve endings on the cells of the pineal gland. The path of regulation of secretion begins from the retina of the eye through the retino-hypothalamic tract, from the interstitial medulla along the preganglionic fibers to the superior cervical sympathetic ganglion, from where the processes of postganglionic cells reach the pineal gland. Thus, a decrease in illumination increases the release of norepinephrine and the secretion of melatonin. In humans, 70% of daily melatonin production occurs at night.

Adrenergic control of melatonin secretion is also possible directly from the hypothalamic structures, which is reflected in the stimulation of melatonin secretion under stress.

The main physiological effect of melatonin is to inhibit the secretion of gonadotropins both at the level of neurosecretion of hypothalamic liberins and at the level of the adenohypophysis. The action of melatonin is realized through the cerebrospinal fluid and blood. In addition to gonadotropins, under the influence of melatonin, the secretion of other adenohypophysis hormones - corticotropin and somatotropin - is reduced to a lesser extent.

The secretion of melatonin is subject to a clear daily rhythm, which determines the rhythm of gonadotropic effects and sexual function. The activity of the pineal gland is often called the “biological clock” of the body, because gland provides processes of temporary adaptation of the body. Administration of melatonin to humans causes

slight euphoria and sleep.

Hormonal function of the gonads.

Male sex hormones .

Male sex hormones - androgens - are formed in Leydig cells of the testes from cholesterol. The main androgen in humans is testosterone . . Small amounts of androgens are produced in the adrenal cortex.

Testosterone has wide range metabolic and physiological effects: ensuring the processes of differentiation in embryogenesis and the development of primary and secondary sexual characteristics, the formation of central nervous system structures that ensure sexual behavior and sexual functions, a generalized anabolic effect that ensures the growth of the skeleton, muscles, the distribution of subcutaneous fat, ensuring spermatogenesis, nitrogen retention in the body , potassium, phosphate, activation of RNA synthesis, stimulation of erythropoiesis.

Androgens are also produced in small quantities in female body, being not only precursors for estrogen synthesis, but also supporting sexual desire, as well as stimulating hair growth on the pubis and armpits.

Female sex hormones .

The secretion of these hormones ( estrogen) is closely related to the female reproductive cycle. The female reproductive cycle provides clear integration over time of the various processes necessary for the implementation reproductive function- periodic preparation of the endometrium for embryo implantation, egg maturation and ovulation, changes in secondary sexual characteristics, etc. The coordination of these processes is ensured by fluctuations in the secretion of a number of hormones, primarily gonadotropins and sex steroids. The secretion of gonadotropins is carried out as “tonic”, i.e. continuously and “cyclically”, with periodic release of large quantities of folliculin and luteotropin in the middle of the cycle.

The sexual cycle lasts 27-28 days and is divided into four periods:

1) preovulatory - the period of preparation for pregnancy, the uterus at this time increases in size, the mucous membrane and its glands grow, the contraction of the fallopian tubes and the muscular layer of the uterus intensifies and becomes more frequent, the vaginal mucosa also grows;

2) ovulatory- begins with the rupture of the vesicular ovarian follicle, the release of the egg and its movement through the fallopian tube into the uterine cavity. During this period, fertilization usually occurs, the sexual cycle is interrupted and pregnancy occurs;

3) post-ovulation- in women during this period, menstruation appears, the unfertilized egg, which remains alive in the uterus for several days, dies, tonic contractions of the muscles of the uterus increase, leading to the rejection of its mucous membrane and the release of fragments of the mucous membrane along with blood.

4) rest period- occurs after the end of the post-ovulation period.

Hormonal changes during the sexual cycle are accompanied by the following changes. In the preovulation period, first there is a gradual increase in the secretion of follitropin by the adenohypophysis. The maturing follicle produces an increasing amount of estrogens, which, through feedback, begins to reduce the production of follinotropin. An increasing level of lutropin leads to stimulation of the synthesis of enzymes, leading to thinning of the follicle wall necessary for ovulation.

During the ovulation period, there is a sharp surge in the level of lutropin, follitropin and estrogens in the blood.

In the initial phase of the postovulation period, there is a short-term drop in the level of gonadotropins and estradiol , the ruptured follicle begins to fill with luteal cells, and new blood vessels are formed. Products are increasing progesterone the resulting corpus luteum, the secretion of estradiol by other maturing follicles increases. The resulting level of progesterone and estrogen feedback suppresses the secretion of follotropin and luteotropin. Degeneration of the corpus luteum begins, the level of progesterone and estrogen in the blood drops. In the secretory epithelium without steroid stimulation, hemorrhagic and degenerative changes, which leads to bleeding, rejection of the mucous membrane, contraction of the uterus, i.e. to menstruation.

Hormonal function of the placenta. . The placenta is so closely functionally related to the fetus that it is customary to use the term “fetoplacental complex.” For example, synthesis in the placenta estriol comes from the precursor of dehydroepiandrosterone produced by the fetal adrenal glands. By the mother's excretion of estriol, one can even judge the viability of the fetus.

The placenta produces progesterone , the effect of which is predominantly local. It is with placental progesterone that the time interval between the births of twins is associated.

One of the main placental hormones is chorionic gonadotropin , which has an effect not only on the processes of differentiation and development of the fetus, but also on metabolic processes in the mother’s body. Chorionic gonadotropin ensures the retention of salts and water in the mother’s body, stimulates the secretion of vasopressin and itself has antidiuretic properties, and activates immune mechanisms.