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Regulation of Activity of Endocrine Glands


Activity of the endocrine glands is regulated by signal (input) and by deviation (quantity). We have already examined the mechanism of regulation by quantity when we discussed regulation of the activity of hormone-producing cells. Now let us look at the 2nd type of regulation – by “input”. Regulation of endocrine glands by input (entry) is realized through neural and humoral mechanisms. An illustration of the neural mechanism is activation of the adrenal medulla in case of stimulation of sympathetic NS with participation of dorsal hypothalamic nuclei of the diencephalon. The humoral mechanism of activation of pituitary-dependent endocrine glands also starts in the hypothalamic region where appropriate releasing hormones (liberins) are secreted. These hormones activate cells of the anterior pituitary (adenohypophysis) to produce tropic hormones, which in turn activate pituitary-dependent endocrine glands. This route of activation is effective in relation to the adrenal cortex.

Action on an organism of a strong stimulus activates not only sympatho-adrenal complex, but also the neurosecretory activity of cells of the hypothalamus, and, particularly, promotes secretion of corticoliberin hormone. This hormone is carried with the bloodstream to the anterior pituitary where it activates synthesis and secretion of adrenocorticotropic hormones. The latter are transported throughout the body and “find” target cells in the adrenal cortex, which respond to this by activation of synthesis and secretion of corticosteroids, in particular, of hydrocortison.

Both mechanisms of regulation of the activity of endocrine glands are complementary and act at different stages of adaptation of the body to varying environment.

In each cell there usually function different kinds of receptors to one hormone (for example, both α- and β-adrenoreceptors). Besides, a cell is usually sensitive to 7-10 different endocrine regulators (neurotransmitters, hormones, prostaglandins, growth factors). Each of these regulators is characterized by specific duration and amplitude of regulatory signal, and each regulator is characterized by a certain proportion of activities of second messenger generation systems in the cell or by certain variations in the membrane potential. At the level of effector systems of the cell there may occur both potentiation and mutual extinction of different regulator signals.

Besides, in each cell there also function special biochemical mechanisms that regulate sensitivity of the cell to a hormone. Let us illustrate these mechanisms on an example of a receptor coupled with G-proteins. The level of hormones that act through this system of transmembrane signalization (which, besides substances mentioned above, include prostaglandins, pituitary hormones, angiotensin II, bradykinin, vasopressin, oxytocin, histamine, dopamine, enkephalin, endorphin, serotonin, endothelin, cholecystokinin, gastrin, parathyroid hormone) usually rises for several minutes. This period is sufficient for formation of the required quantity of the second messengers (cyclic AMP, Ca2+, diacylglycerole), which activate the respective protein kinases with subsequent phosphorylation of proteins. But if the level of hormones stays high for dozens of minutes or several hours (due to hyperfunction of the endocrine gland or to pharmacological intervention), the desensitization of the respective receptor results. At first the receptor becomes phosphorylated by protein kinase present in the plasma membrane practically of all cells, which decreases their affinity to this hormone 2-5-fold. This protein kinase may phosphorylate only hormone+receptor complex; therefore the longer the hormone remains bound to the receptor, the higher the probability for this receptor to be phosphorylated. If such phosphorylation is unable to suppress the hormone signal, then 15-30 minutes later the receptor becomes phosphorylated by protein kinase that is activated by the respective second messenger (for example, by cAMP-dependent protein kinase in case of β-adrenergic receptors that activate adenylate cyclase; or by protein kinase C in case of α1-adrenergic or M1- and M3-cholinergic receptors that activate phospholipase C). Phosphorylation of receptors by protein kinases dependent on second messengers, deranges coupling with G-proteins that weakens activating or inhibiting influence of hormones acting through receptors on adenylate cyclase or K+ channels. If the level of the hormone remains high within hours, and the above mentioned desensitization mechanisms cannot suppress the regulatory signal, the hormone+receptor complexes undergo endocytosis, with receptorosomes appearing inside cells. If the level of hormone decreases within the first 2-3 hours, they may again build into the plasma membrane. If the level does not decrease, they fuse with the lysosomes, after which receptors become disrupted. It is clear that restoration of the sensitivity of the cell to this hormone will require new synthesis of hormones.

Date: 2015-01-02; view: 1054

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