Function of the posterior lobe of the pituitary gland

Function of the posterior lobe of the pituitary gland

Function of the posterior lobe of the pituitary gland



The posterior lobe of the pituitary gland produces antidiuretic hormone (aka vazopressin) and oxytocin. Both hormones are released in response to neural impulses and have a half-life of about 10 minutes.


Antidiuretic hormone (ADH). ADH mainly causes a delay in the excretion of water by the kidneys, increasing the permeability of the distal tubular epithelium to water. In high concentrations, ADH also causes vasoconstriction. Like aldosterone, ADH plays an important role in maintaining water-electrolytic homeostasis, vascular and cellular hydration. The main reason for the release of ADH is an increase in the osmotic pressure of water in the body, which is perceived by the osmoreceptors of the hypothalamus. Another important reason is the reduction of the BCC, which causes irritation of the baroreceptors in the left atrium, pulmonary veins, carotid sinus, aortic arch and is transmitted to the CNS through the vagus and glossopharyngeal nerves. Other stimulants for increasing ADH are pain,stress, vomiting, hypoxia, exercise, hypoglycemia, cholinergic agonists, blockers, angiotensin, and prostaglan-din. The inhibitors of ADH are alcohol, β-blockers and glucocorticoids.


Lack of ADH productsleads to central diabetes insipidus; when the kidney is unable to respond to normal ADH, nephrogenic diabetes insipidus develops. Removal of the pituitary gland, as a rule, does not change the course of non-diabetes mellitus, as hypothalamic neurons remain, producing small amounts of ADH.


Oxytocin. Oxytocin has 2 main targets: the myoepithelial cells of the mammary glands, which surround the alveoli of the mammary glands, and the smooth muscle cells of the uterus. Sucking stimulates oxytocin production as a result of reduction of myo-epithelial cells. This reduction leads to the movement of milk from the alveoli to the large sinuses for emptying (for example, excretion of milk from breastfeeding mothers). Oxytocin stimulates the reduction of smooth muscle cells of the uterus, and the sensitivity of the uterus to oxytocin increases during pregnancy. But during childbirth, the level of the hormone in the plasma does not increase dramatically, and the role of oxytocin in stimulating labor activity requires clarification.There are no established stimuli (or functions) for the secretion of oxytocin in men who show an extremely low level of the hormone of the endocrine glands, arising independently (primary disorders) or with insufficient or excessive stimulation by the pituitary (secondary disorders). Disorders can be the result of increased (hyperfunction) or reduced production (hypofunction) of the hormone. Rarely endocrine disorders (usually hypofunction) arise due to inadequate response of tissues to the hormone. Clinical signs of hypofunctional disorders develop most often gradually and are non-specific.


Hyperfunction.Hyperfunction of the endocrine glands may be the result of excessive stimulation by the pituitary gland, but is generally the result of hyperplasia or neoplasia of the gland itself. In some cases, cancers from other tissues can produce hormones (ectopic hormone production). Excess hormone may be the result of exogenous administration of the hormone. In some cases, patients take hormones without the advice of a physician (artificial disease).There is a hypersensitivity of tissues to hormones. Antibodies can stimulate peripheral endocrine glands, which is observed in hyperthyroidism (Graves' disease). The destruction of peripheral endocrine glands can lead to a rapid release of the hormone (eg, thyroid hormones in destructive thyroiditis). Enzyme deficiencies in the synthesis of peripheral endocrine hormones may be the result of increased production of hormones proximally (higher) than the block. Finally, increased hormone production can cause both an adequate response and a state of illness.


Hypofunction.The hypofunction of the endocrine glands can be the result of reduced stimulation by the pituitary gland. Hypofunction occurs within the peripheral gland independently as a result of congenital or acquired disorder (including autoimmune conditions, tumors, infections, vascular diseases and toxins). Genetic disorders that cause hypofunction may be the result of a deletion of a gene or in the production of a pathological hormone. Reduced production of the hormone by the peripheral endocrine gland with increased formation of the regulatory hormone of the pituitary gland can lead to hyperplasia of the peripheral endocrine gland.For example, if the synthesis of thyroid hormones is impaired, the thyroid-stimulating hormone (TSH) is produced in an excess amount, causing a goiter.


Some hormones require transformation into the active form after secretion by the peripheral endocrine gland. Certain disorders can block this stage (for example, kidney diseases can inhibit the production of active forms of vitamin D). Antibodies against the hormone circulating in the blood or its receptor can block the hormone's ability to bind to the receptor. Disease or medication can cause an increase in the intensity of hormone clearance. The substances circulating in the blood may also block the function of hormones. Anomaly of the receptor or a violation of other localization in the peripheral endocrine tissue can also lead to hypofunction.


Laboratory research


Since the symptoms of endocrine disorders can develop gradually and are non-specific, clinical diagnosis is often delayed for months or years. For this reason, biochemical diagnosis is usually irreplaceable; The classic requirement is to determine the levels of peripheral endocrine hormones and / or pituitary hormones in the blood.


Free or bioactive hormone(for example, not associated with a specific protein) is crucial for the formation of the active form. Free or bioactive hormones are determined using equilibrium dialysis, ultrafiltration, or a solvent extraction method to separate free or albumin-bound hormone from bound globulin. These methods can be expensive and lengthy. A similar and competitive definition of free hormone, often using commercial kits, does not always give a reliable result and should not be used.


Free hormone levelscan also be determined indirectly by estimating levels of bound protein using then determined levels of total serum hormone. However, indirect methods are less reliable if the binding ability of the hormone-bound protein changes (for example, in case of a disease).


Although most hormones have daily rhythms, studies should be performed at the prescribed time of day. Hormones with a very short half-life (for example, luteinizing hormone) make it necessary to use 3 or 4 measurements every 1 or 2 hours or to use several blood samples.Hormones, the level of which changes every week (for example, testosterone), require separate weekly measurements.


In some cases, an indirect estimate is used. For example, somatotropic hormone (STH) has a short half-life in serum and therefore is difficult to measure. Insulin-like serum factor 1 (IGF-1), which is produced in response to the release of GH, is most often used to measure GH activity as an index. Sometimes hormone levels in the urine or saliva can be used (for example, free cortisol, which is determined by Cushing's disease). Regardless of the fact that the quantitative determination of circulating hormone metabolites indicates the amount of bioactive hormone, this problem requires further observation.


In most cases, a dynamic study is necessary. So, in cases of organ hypofunction, a stimulating test can be used. When hyperfunction can be applied suppressive test.


Treatment of function of the posterior lobe of the pituitary gland


Non-functional disorders are usually corrected by taking peripheral endocrine hormones, regardless of whether they are primary or secondary (an exception is the prescription of GH in pituitary ganism).If hormone resistance is observed, drugs can be used to change resistance (for example, metformin or thiazolidine-diones in type 2 diabetes mellitus). Sometimes used hormone stimulating drugs.


For the treatment of hyperfunctional disorders, radiation therapy, surgical interventions and medications that suppress hormone production are used. In some cases, receptor antagonists are used.

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