The role of steroid hormones, thyroid and parathyroid hormones. Releasing hormones List of hypothalamic hormones, their increase and decrease

Hypothalamic hormone family - releasing factors– includes substances, usually small peptides, formed in the nuclei of the hypothalamus. Their function is the regulation of the secretion of adenohypophysis hormones: stimulation - liberins and suppression - statins.

The existence of seven liberins and three statins has been proven.

Thyroid hormone– is a tripeptide, stimulates the secretion of the thyroid-stimulating hormone iprolactin, and also exhibits antidepressant properties.

Corticoliberin– a polypeptide of 41 amino acids, stimulates the secretion of ACTH and β-endorphin, widely affects the activity of the nervous, endocrine, reproductive, cardiovascular and immune systems.

GnRH(luliberin) – a peptide of 10 amino acids, stimulates the release of luteinizing and follicle-stimulating hormones. GnRH is also present in the hypothalamus, participating in the central regulation of sexual behavior.

Folliberin– stimulates the release of follicle-stimulating hormone.

Prolactoliberin– stimulates the secretion of lactotropic hormone.

Prolactostatin– it is assumed that it is dopamine. Reduces the synthesis and secretion of lactotropic hormone.

Somatoliberin consists of 44 amino acids and increases the synthesis and secretion of growth hormone.

Somatostatin– a peptide of 12 amino acids that inhibits the secretion of TSH, prolactin, ACTH and growth hormone from the pituitary gland. It is also formed in the islets of the pancreas and controls the release of glucagon and insulin, as well as hormones of the gastrointestinal tract.

Melanostimulating factor, a pentapeptide, has a stimulating effect on the synthesis of melanotropic hormone.

Melanostatin, can be either a tri- or pentapeptide, has an anti-opioid effect and activity in behavioral reactions.

In addition to releasing hormones, the hypothalamus also synthesizes vasopressin (antidiuretic hormone) and oxytocin.

Vasopressin and oxytocin - these hormones are conventionally called hormones of the posterior lobe of the pituitary gland, these are true hormones of the hypothalamus, they enter the pituitary gland along the axons and are secreted from there. These are peptides consisting of 9AA residues. They are synthesized from various precursors by the ribosomal route. Mechanism of action: membrane-cytosolic.

Vasopressin is an antidiuretic hormone (ADH). It stimulates the reabsorption of water by the renal tubules, which means it reduces diuresis (urination) and regulates water metabolism. This hormone indirectly regulates mineral metabolism by reducing the concentration of ions in the blood and, accordingly, increasing it in the urine. Vasopresin acts through the adenylate cyclase system; cell membrane proteins are phosphorelated, which sharply increases its permeability to water. Hypofunction or hypoproduction of this hormone leads to the development of “diabetes insipidus”, and diuresis increases accordingly. Vasopressor action Vasopressin regulates blood pressure by constricting peripheral blood vessels, it acts through a membrane-cytosolic mechanism, unlike renal tubular cells, it acts through calcium ions and inositol-3-phosphate, and diacylglycerol. Constriction of blood vessels increases blood pressure.

Oxytocin - stimulates the contraction of the smooth muscles of the uterus, as well as the myoepithelial cells surrounding the alveoli of the mammary ducts, and therefore stimulates lactation. Sensitivity to oxytocin depends on sex hormones: estrogens increase the sensitivity of the uterus to oxytocin, and progesterone decreases it.

Tropic, since their target organs are endocrine glands. Pituitary hormones stimulate a specific gland, and an increase in the level of hormones secreted by it in the blood suppresses the secretion of the pituitary hormone according to the feedback principle.

Thyroid-stimulating hormone (TSH) is the main regulator of the biosynthesis and secretion of thyroid hormones. According to its chemical structure, thyrotropin is a glycoprotein hormone. Thyroid-stimulating hormone consists of two subunits (α and β) connected to each other by a non-covalent bond. The α-subunit is also present in other hormones (phyllitropin, lutropin, human chorionic gonadotropin hormone). Each of these hormones also has a β-subunit, which ensures the specific binding of hormones to their receptors. Thyrotropin receptors are located on the surface of the epithelial cells of the thyroid gland. Thyrotropin, acting on specific receptors in the thyroid gland, stimulates the production and activation of thyroxine. It activates adenylate cyclase and increases iodine consumption by gland cells. biosynthesis of triiodothyronine (T3) and thyroxine (T4) (synthesis lasts about a minute), which are the most important growth hormones. In addition, thyrotropin causes some long-lasting effects that take several days to appear. This is, for example, an increase in the synthesis of proteins, nucleic acids, phospholipids, an increase in the number and size of thyroid cells. In high concentrations and with prolonged exposure, thyrotropin causes proliferation of thyroid tissue, an increase in its size and weight, an increase in the amount of colloid in it, i.e. its functional hypertrophy.

Adrenocorticotropic hormone (ACTH) - stimulates the adrenal cortex. The ACTH molecule consists of 39 amino acid residues. The characteristics of ACTH are determined by various parts of its peptide chain.

The hormone is produced in the cells of the anterior pituitary gland. Secretion is regulated by hypothalamic corticoliberin. Synthesized as a prohormone. Under stress, the concentration of ACTH in the blood increases many times.

The targets of ACTH are the endocrine cells of the zona fasciculata of the adrenal cortex, which synthesize glucocorticoids.

Stimulates the synthesis and secretion of hormones of the adrenal cortex, has fat-mobilizing and melanocyte-stimulating activity. ACTH interacts with specific receptors on the outer surface of the cell membrane. In the cells of the adrenal cortex, ACTH stimulates the hydrolysis of cholesterol esters and increases the entry of cholesterol into the cells; induces the synthesis of mitochondrial and microsomal enzymes involved in the synthesis of corticosteroids. ACTH is capable of melanocyte-stimulating activity.

In high concentrations and with prolonged exposure, corticotropin causes an increase in the size and weight of the adrenal glands, especially their cortex, an increase in the reserves of cholesterol, ascorbic and pantothenic acids in the adrenal cortex, that is, functional hypertrophy of the adrenal cortex, accompanied by an increase in the total content of protein and DNA in them. This is explained by the fact that under the influence of ACTH, the activity of DNA polymerase and thymidine kinase increases in the adrenal glands. Excess ACTH leads to hypercortisolism, i.e. increased production of corticosteroids, mainly glucocorticoids. This disease develops with pituitary adenoma and is called Itsenko-Cushing's disease. Its main manifestations are: hypertension, obesity, which is local in nature (face and torso), hyperglycemia, decreased immune defense of the body.

Lack of the hormone leads to a decrease in the production of glucocorticoids, which is manifested by metabolic disorders and a decrease in the body’s resistance to various environmental influences.

Gonadotropic hormones:

· follicle-stimulating hormone (FSH) - promotes the maturation of follicles in the ovaries, simulating endometrial proliferation.

luteinizing hormone (LH) - causes ovulation and the formation of the corpus luteum.

Glycoproteins consist of alpha and beta chains. The target is the gonads. FSH regulates the maturation of germ cells, the growth of follicles, the formation of follicular fluid, and induce ovulation. LH increases the synthesis of proestrogens, the production of cAMP, promotes ovulation, and stimulates the synthesis of progesterone. Hyperfunction leads to premature puberty, disorders of the sexual cycle, hypofunction leads to excess estrogen.

Somatotropic hormone (GH) is the most important stimulator of protein synthesis in cells, glucose formation and fat breakdown, as well as body growth. Causes a pronounced acceleration of linear (lengthwise) growth, mainly due to the growth of long tubular bones of the limbs. Somatotropin has a powerful anabolic and anti-catabolic effect, enhances protein synthesis and inhibits its breakdown, and also helps reduce the deposition of subcutaneous fat, enhance fat burning and increase the ratio of muscle mass to fat. In addition, somatotropin takes part in the regulation of carbohydrate metabolism - it causes a pronounced increase in blood glucose levels and is one of the counter-insular hormones, insulin antagonists in their effect on carbohydrate metabolism.

Receptors for the hormone are located on the somatic membrane of the liver, testicles, lungs, and brain.

Excess

In adults, a pathological increase in the level of somatotropin or long-term administration of exogenous somatotropin in doses characteristic of a growing organism leads to thickening of the bones and coarsening of facial features, an increase in the size of the tongue - macroglossia. Associated complications include compression of nerves (tunnel syndrome), decreased muscle strength, and increased tissue insulin resistance. The usual cause of acromegaly is an adenoma of the anterior pituitary gland. Typically, adenomas occur in adulthood, but in rare cases of their occurrence in childhood, pituitary gigantism is observed.

Flaw

Lack of growth hormone in childhood is associated mainly with genetic defects and causes growth retardation, pituitary dwarfism, and sometimes also puberty. Mental retardation appears to be observed with polyhormonal insufficiency associated with underdevelopment of the pituitary gland. In adulthood, growth hormone deficiency causes increased deposition of body fat.

Luteotropic hormone (prolactin) - regulates lactation, differentiation of various tissues, growth and metabolic processes, instincts of caring for offspring. . Its chemical structure is a peptide hormone. The main target organ of prolactin is the mammary glands. Prolactin is necessary for lactation, it increases the secretion of colostrum, promotes the maturation of colostrum, and the transformation of colostrum into mature milk. It also stimulates the growth and development of the mammary glands and an increase in the number of lobules and ducts in them. In addition to the mammary glands, prolactin receptors are found in almost all other organs of the body, but the effect of this hormone on them is not yet known. Prolactin is responsible for inhibiting the ovulation cycle by inhibiting the secretion of follicle-stimulating hormone (FSH) and gonadotropin-releasing factor (GnTR). In women, prolactin helps prolong the existence of the corpus luteum of the ovaries (lengthening the luteal phase of the cycle), inhibits ovulation and the onset of a new pregnancy, reduces the secretion of estrogen by ovarian follicles and the secretion of progesterone by the corpus luteum.

The condition of elevated levels of prolactin in the blood is called hyperprolactinemia. There are two types of hyperprolactinemia: physiological and pathological. Physiological hyperprolactinemia is not associated with disease. The concentration of prolactin may increase during deep sleep, intense physical activity, breastfeeding, pregnancy, sexual intercourse, and stress. Pathological hyperprolactinemia is usually caused by some disease. With hyperprolactinemia in women, the menstrual cycle is disrupted. An increase in the concentration of prolactin can lead to the development of infertility, anorgasmia, frigidity, a decrease in the level of sexual desire, an increase in the size of the mammary glands up to the formation of macromastia (giant mammary glands), cysts or adenomas of the mammary glands can develop, and subsequently even breast cancer.

The hypothalamus serves as a place of direct interaction between the higher parts of the central nervous system and the endocrine apparatus. The nature of the connections that exist between the central nervous system and the endocrine system began to be clarified in the last decade, when the first humoral factors, called mediators, were isolated from the hypothalamus and turned out to be hormonal substances with extremely high biological activity. It took a lot of work and experimental skill to prove that these substances 1 are formed in the nerve cells of the hypothalamus, from where they reach the pituitary gland through the portal capillary system, regulating the secretion of pituitary hormones, or rather their release (and, possibly, biosynthesis); these substances were first called neurohormones, and then releasing factors (from the English release - to free); substances with the opposite effect, i.e., inhibiting the release (and, possibly, biosynthesis) of pituitary hormones, are called inhibitory factors. Thus, the hormones of the hypothalamus play a key role in the physiological system of hormonal regulation of the multilateral biological functions of individual organs, tissues and the whole organism.

1 For the first time, Guillemin and Shely succeeded in the early 70s in isolating substances from hypothalamic tissue that had a regulating effect on the function of the pituitary gland. These authors, together with Llow, who developed the radioimmunological method for determining peptide hormones, were awarded the Nobel Prize in 1977 for the discovery of the so-called superhormones.

The above can be illustrated in the form of the following diagram (according to N. A. Yudaev and Z. F. Utesheva):

To date, seven stimulators (releasing hormones) and three inhibitors (inhibiting factors) of pituitary hormone secretion have been discovered in the hypothalamus. Of these, only three hormones have been isolated in their pure form, for which their structure has been established and confirmed by chemical synthesis.

It is impossible not to point out one important circumstance that can explain the difficulties of obtaining hypothalamic hormones in their pure form - their extremely low content in the original tissue. Thus, to isolate only 1 mg of thyrotropin-releasing factor (according to the new nomenclature - thyrotropin-releasing hormone, see Table 20), it was necessary to process 7 tons of hypothalamus obtained from 5 million sheep. In table 20 shows the currently discovered hypothalamic hormones.

It should be noted that not all hypothalamic hormones appear to be strictly specific to any one pituitary hormone. In particular, the ability to release thyrotropin-releasing hormone, in addition to thyrotropin, also prolactin, and for luliberin, in addition to luteinizing hormone, also follicle-stimulating hormone.

Table 20. Hypothalamic hormones that control the release of pituitary hormones
Old name Accepted abbreviations New working title 1
Corticotropin releasing factorKRF, KRGCorticoliberin
Thyrotropin-releasing factorTRF, TRG
Luteinizing hormone releasing factorLGRF, LGRG, LRF, LRGLuliberin
Follicle-stimulating hormone releasing factorFRF, Germany, FSG-RF, FSG-RGFolliberin
Somatotropin-releasing factorSRF, SRGSomatoliberin
Somatotropin inhibitory factorCIFSomatostatin
Prolactin releasing factorPRF, PRGProlactoliberin
Prolactininhibiting factorMutual Fund, PIGProlactostatin
Melanotropin-releasing factorMRF, MWGMelanoliberin
Melanotropin inhibitory factorMYTH, MIGMelanostatin
1 Hypothalamic hormones do not have firmly established names. As you can see, it is recommended to add the ending “liberin” to the prefix of the name of the released pituitary hormone, for example, “thyroliberin” means a hypothalamic hormone that stimulates the release (and, possibly, synthesis) of thyrotropin, the corresponding pituitary hormone. The names of hypothalamic factors that inhibit the release (and possibly synthesis) of pituitary tropic hormones are formed in a similar way, with the addition of the ending “statin”. For example, "somatostatin" means a hypothalamic peptide that inhibits the release (synthesis) of pituitary growth hormone - somatotropin.

Regarding the chemical structure of the hypothalamic hormones, as stated above, it has been established that all of them are low molecular weight peptides, so-called oligopeptides of unusual structure, although the exact amino acid composition and primary structure have been clarified for only three of them: thyroliberin (promoting the release of thyrotropin), luliberin (promoting release of luteinizing hormone) and somatostatin (which has an inhibitory effect on the release of growth hormone - somatotropin). Below is the primary structure of all three hormones:

  1. Thyroliberin (Piro-Glu-Gis-Pro-NNH 2). It can be seen that thyroliberin is represented by a tripeptide consisting of pyroglutamic (cyclic) acid, histidine and prolinamide connected by peptide bonds; unlike classical peptides (see Protein Chemistry), it does not contain free NH 2 - and COOH groups at the N- and C-terminal amino acids.
  2. Luliberin is a decapeptide consisting of 10 amino acids in the following sequence: Pyro-Glu-Gis-Tri-Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH 2 ; the terminal C-amino acid is glycinamide.
  3. Somatostatin is a cyclic tetradecapeptide (consisting of 14 amino acid residues). This hormone differs from the two previous ones, in addition to the cyclic structure, in that it does not contain pyroglutamic acid at the N-terminus of the peptide, but includes a free NH 2 group of alanine, as well as a free COOH group of cysteine ​​at the C-terminus; a disulfide bond is formed between two cysteine ​​residues at the 3rd and 14th positions. Its complete chemical synthesis was carried out in a number of laboratories, including in 1979 at the Institute of Experimental Endocrinology and Chemistry of Hormones of the USSR Academy of Medical Sciences. It should be noted that the synthetic linear analogue of somatostatin is also endowed with similar biological activity, which indicates the insignificance of the disulfide bridge of the natural hormone. In addition to the hypothalamus, somatostatin is also found in other parts of the brain, in the pancreas, and intestinal cells; it has a wide range of biological effects, in particular, its direct effect on the cellular elements of the islets of Langerhans and the adenohypophysis has been shown.

    In addition to the listed hypothalamic hormones, obtained in pure form and confirmed by synthesis, two purified preparations were isolated from hypothalamic tissue that stimulate the release of growth hormone; they differ from each other in a number of properties, as well as in molecular weight, although they have almost the same biological activity. The chemical nature of another hormone, corticotropin-releasing factor, has been intensively studied. Its active preparations were isolated both from the tissue of the hypothalamus and from the posterior lobe of the pituitary gland (neurohypophysis); there is an opinion that it can serve as a depot for it, just as it serves as a depot for vasopressin and oxytocin. It is assumed that corticoliberin is a polypeptide, but its exact structure has not yet been elucidated. The chemical nature of other hypothalamic hormones is also not determined. Work on isolating and identifying releasing factors is currently in full swing. The scale of such work and the difficulties associated with it are evidenced by the fact that in order to isolate milligrams of any hypothalamic hormone, the Laboratory processes the brains of hundreds of thousands and even millions of sheep.

    Available data regarding the location and mechanism of biosynthesis of hypothalamic hormones indicate that the site of synthesis is most likely the nerve endings - synaptosomes of the hypothalamus, since these formations contain the highest concentration of hormones and biogenic amines; the latter are considered along with the hormones of the peripheral endocrine glands, acting on the feedback principle, as the main regulators of the secretion and synthesis of hypothalamic hormones. The mechanism of biosynthesis of thyroliberin, most likely carried out by a non-ribosomal route, includes the participation of an SH enzyme (called TRP synthetase) or a complex of enzymes that catalyze the cyclization of glutamic acid into pyroglutamic acid, the formation of a peptide bond and the amidation of proline in the presence of glutamine. The existence of a similar biosynthesis mechanism with the participation of corresponding synthetases is also assumed for luliberin and somatoliberin.

    The pathways for inactivation of hypothalamic hormones have not been sufficiently studied. The half-life of thyrotropin-releasing hormone in rat blood is 4 minutes. Inactivation occurs both when the peptide bond is broken (under the influence of exo- and endopeptidases from rat and human blood serum) and when the amide group in the prolinamide molecule is removed. In addition, a specific enzyme, pyroglutamyl peptidase, has been discovered in the hypothalamus of humans and a number of animals, which catalyzes the cleavage of the pyroglutamic acid molecule from thyroliberin and luliberin.

    Data on the mechanism of action of hypothalamic hormones indicate both their direct influence on the secretion (more precisely, release) of “ready” pituitary hormones, and on their de novo biosynthesis. Evidence has been obtained of the participation of cyclic AMP in the transmission of hormonal signals. The existence of specific adenohypophyseal receptors in the plasma membranes of pituitary cells has been shown, with which hypothalamic hormones bind and through the system of adenylate cyclase and membrane complexes Ca 2+ - ATP and Mg 2+ - ATP, Ca 2+ and cAMP ions are released; the latter acts on both the release and synthesis of the corresponding pituitary hormone by activating protein kinase (see below).

It secretes hormones that control the endocrine system. Secretory activity occurs through hypothalamic neurons. In general, we can say that all nerve cells secrete hormones. They are capable of producing acetylcholine, norepinephrine and dopamine, which work in the body as mediators, that is, they take part in the transmission of various nerve impulses.

The hypothalamus contains the supraoptic and paraventricular nuclei. They secrete, responsibly, vasopressin and oxytocin. These hormones, together with the carrier protein, enter the posterior lobe of the pituitary gland through the pituitary stalk, and it has a common neurogenic origin with the hypothalamus, but is at the same time a depot where these hormones only accumulate, but they are not produced there.

What hormones does the hypothalamus secrete?

Other parts of the hypothalamus produce hypophysiotropic hormones (they are often also called releasing factors). They control the release of hormones from the anterior pituitary gland. This part of the pituitary gland does not embryologically belong to the brain, and at the same time does not have direct innervation from the hypothalamus.

It is connected to the hypothalamus by a network of vessels that runs along the pituitary stalk. Releasing hormones enter the anterior lobe of the pituitary gland through the blood vessels, regulating the synthesis and release of various pituitary hormones. The regulation of such hormones is carried out by stimulating and at the same time various inhibitory hormones of the hypothalamus.

But in relation to some groups of pituitary hormones, their regulation by stimulating releasing hormones is of greater importance, while another is the influence of inhibitory hormones of the hypothalamus. In this case, the first group of hormones includes ACTH, TSH (thyrotropin), STH (growth hormone), FSH and LH. Each of them is regulated by corresponding hypothalamic releasing hormones.

At this point in time, the structures of TSH-RH (that is, thyrotropin-releasing hormone), which turned out to be a tripeptide, as well as STH-RH, ACTH-RH and LH-RH, which have the structure of decapeptides, have been deciphered.

Using synthetic TSH-RG, when administered intravenously in a healthy person, the concentration of thyrotropin in the blood can be significantly increased. MSH and prolactin are regulated primarily by inhibitory hypothalamic factors, MIF and PIF, respectively. Therefore, in the case of transection of the pituitary stalk, when the influence of the hypothalamus is eliminated, the secretion of prolactin and MSH increases, and the secretion of other pituitary hormones at the same time sharply decreases.

What else can the hypothalamus do?

In addition to neurosecretory activity, some clusters of hypothalamic neurons also play the role of neurogenic centers that regulate some basic functions of the body. In particular, the thirst center is located in the hypothalamus. At the same time, neurophysiological data show that the feeling of thirst manifests itself as hypothalamic signals in response to an increase in the level of osmotic blood pressure (blood thickening), which is perceived by the osmoreceptors of the hypothalamic supraoptic nucleus.

As a result of this effect, which changes the electrical properties of the membranes of osmoreceptors, the secretion of the hormone vasopressin increases, and as a result, water retention in the body is achieved.

At the same time, a feeling of thirst appears, which is ultimately aimed at restoring osmotic pressure. Receptors that are located in different parts of the vascular bed also simultaneously perceive changes in the volume of circulating blood in the body. Information enters both the hypothalamus and at the same time the renin-angiotensin system. This, along with the effect of angiotensin on the hypothalamus, has a regulatory effect through the kidneys.

In addition to the thirst center, the hypothalamus contains thermoreceptors that sense changes in blood temperature. In this case, there are separate neurons that respond to decreases and increases in temperature (hypothalamic thermoregulation occurs).

It is important to mention that serotonin and catecholamines, influencing the hypothalamic thermoregulation center, can change body temperature.

Hypothalamic regulation of appetite in humans is associated primarily with the lateral and ventromedial parts of the hypothalamus. They work respectively as an “appetite center” (hunger) and a “satiety center.”

Previously, it was believed that energy-temperature, lipostatic and osmotic mechanisms regulate the activity of these centers in the body, but now it is believed that the regulation of the processes of appetite and satiety is regulated by the glucostatic mechanism.

In this case, the main role is played primarily not only by the absolute level of glucose in one or another part of the hypothalamus, where glucoreceptors are located, but by the intensity of glucose utilization in these receptors.

It should be emphasized that during hypoglycemia, for example, in the case of excess insulin in the body, appetite stimulation is also carried out due to the activation of secondary behavioral reactions.

Even more important is that not only the state of the appetite center, but also the regulation of GH secretion, which is of key importance in providing the body with energy substrates, is related to the process of glucose utilization. It is also possible that the hypothalamus receives information about how intensively glucose is utilized in the periphery, primarily in the liver.

The regulation of sleep and wakefulness is also associated with the activity of the hypothalamus. But here, as well as in relation to the regulation of emotional manifestations, the hypothalamus manifests itself more as an integral part of the reticular formation that controls these manifestations.

The hypothalamus also plays a significant role in the processes of regulating the cardiovascular system. The role of hypothalamic disorders, for example, increased activity of vasoregulatory centers in the further development of hypertension, is undoubted. The same can be said about the regulation of the body’s autonomic functions.

Although it is carried out by different parts of the central nervous system, the hypothalamus has a dominant effect. It is characteristic that the signs of sympathetic activation, which occurs when the hypothalamus is irritated, then extend to the cardiovascular system and the functional state of the whole organism.

The pituitary part of the hypothalamus and the effect on the body of hypothalamic neurons in the hypothalamic centers are under the control of neurotransmitters formed mainly in the hypothalamus itself. The nerve endings of hypothalamic neurons differ in their specialization in the secretion of the hormones dopamine, norepinephrine and serotonin.

Adrenergic neurons increase the secretion of various releasing hormones and, as a result, the secretion of ACTH, gonadotropic hormones, prolactin and growth hormone and suppress the secretion of inhibitory hormones of the hypothalamus.

Therefore, reserpine and aminazine, which can block adrenergic impulse transmission, affect the decrease in the secretion of gonadotropins. ACTH and STH, on the contrary, increase the secretion of gonadotropins as a result of suppression of the secretion of PIF. Moreover, DOPA, being a precursor of norepinephrine and dopamine, increases the concentration of catecholamines in the brain and therefore inhibits the secretion of the hormone prolactin, but at the same time increases the production of gonadotropins, growth hormone, and TSH.

But it should be noted that the data showed that norepinephrine-producing and dopamine-producing neurons, despite their adrenergic nature, in the hypothalamus often have separate, specific functions. Thus, norepinephrine-producing neurons also control the secretion of vasopressin and oxytocin. Serotonin-producing neurons are similarly associated with mechanisms that control the secretion of ACTH and gonadotropins, and the concentration of serotonin in the brain reduces the production of gonadotropins, such as LH.

This explains the fact that imipramine, which blocks serotonin transport, affects changes in the estrous cycle, and -ethyl-tryptamine, which activates serotonin receptors, reduces the secretion of the hormone ACTH. Melatonin and some other methoxyindoles affect the hypothalamus, acting at the level of serotonin-producing neurons, causing a decrease in the secretion of MSH, gonadotropins, a decrease in thyroid function and stimulate the “sleep center”.

Hypothalamic hormones

Hypothalamic hormones- the most important regulatory hormones produced by the hypothalamus. All hypothalamic hormones have a peptide structure and are divided into 3 subclasses: releasing hormones stimulate the secretion of hormones of the anterior lobe of the pituitary gland, statins inhibit the secretion of hormones of the anterior lobe of the pituitary gland, and hormones of the posterior lobe of the pituitary gland are traditionally called hormones of the posterior lobe of the pituitary gland according to the place of their storage and release, although are actually produced by the hypothalamus.

Hormones of the hypothalamus play one of the leading roles in the activities of the entire human body. These hormones are produced in a part of the brain called the hypothalamus. Without exception, all of these substances are peptides. Moreover, all these hormones are divided into three types: releasing hormones, statins and hormones of the posterior pituitary gland. The subclass of hypothalamic releasing hormones includes the following hormones:

The subclass of hormones of the posterior lobe of the pituitary gland includes:

  • antidiuretic hormone, or vasopressin

Vasopressin and oxytocin are synthesized in the hypothalamus and then released to the pituitary gland. Secretion regulation function.


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The hypothalamus is a section of the brain located below the thalamus (thalamus - “visual hillocks”, clusters of nerve cells in the brain between the midbrain and the cerebral cortex). The role of the hypothalamus is that it is the highest center of hormonal regulation, combining endocrine and nervous regulatory mechanisms into a single neuro-endocrine system. Neurohormones of the hypothalamus have a long-term regulatory effect on all organs and functions of the body.

Location.

A section of the diencephalon located at the base of the brain.

Functions.

The vegetative center, which coordinates the activities of various internal systems, adapting them to the integrity of the whole organism.

  • Maintains an optimal level of metabolism (protein, carbohydrate, fat, water, mineral) and energy.
  • Regulates the temperature balance of the body.
  • Regulates the activity of the digestive, cardiovascular, excretory and respiratory systems.
  • Controls the activity of all endocrine glands.

Structure and dimensions.

The mass of the hypothalamus is about 4 g. Groups of cells form 32 pairs of nuclei. The hypothalamus is divided into anterior, middle and posterior lobes.

Microstructure.

  • The anterior lobe contains the supra-optic nucleus, which produces vasopressin and oxytocin.
  • The middle lobe contains the ventromedial nuclei, which are considered the center of satiety and the center of hunger.
  • The medial and lateral nuclei of the mastoid body are located in the posterior lobe of the hypothalamus. The posterior hypothalamus provides heat transfer.
  • In addition, the anterior lobe of the hypothalamus contains the sleep center, neurons sensitive to heat and cold.

Hormones of the hypothalamus.

Liberins are hormones of the hypothalamus that activate and stimulate the release of tropic hormones of the pituitary gland (tropic hormones are hormones of the anterior pituitary gland, which in turn stimulate the work of the peripheral endocrine glands)

  • Corticotropin releasing hormone ACTH (CRH). – stimulates the release of adrenocorticotropic hormone
  • Thyrotropin-releasing hormone (TRH) – stimulates the release of the thyroid-stimulating hormone TSH
  • Luteinizing hormone-releasing hormone (LH-RH).
  • Folliberine-releasing hormone-follicle-stimulating hormone (FSH-RH).
  • Somatotropin-releasing hormone (SRH).
  • Prolactoliberin-prolactin-releasing hormone (PRH).
  • Melanoliberin-releasing hormone-melanostimulating hormone (MRH)

Statins have a inhibitory effect on the release of pituitary tropic hormones.

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