Vasopressin physiological effect

Vasopressin is a peptide hormone produced by the hypothalamus and secreted by the posterior pituitary in response to stimulation. Normal stimuli for vasopressin release are hyperosmolarity and hypovolemia, with thresholds for secretion of greater than 280 mOsm/kg and greater than 20% plasma volume depletion. A number of other stimuli, such as pain, nausea, epinephrine, and numerous drugs, induce release of vasopressin. Vasopressin release is inhibited by volume expansion, ethanol, and norepinephrine. The physiological effect of vasopressin is to promote free water clearence by altering the permeability of the renal collecting duct to water. In addition, it has a direct vasoconstrictor effect. Consequently, vasopressin results in water retention and volume restoration. In patients with septic shock, vasopressin is appropriately secreted in response to hypovolemia and to elevated serum osmolarity (R14). 

Bradykinin, vasopressin, and oxytocin are peptide hormones. They are all nonapeptides. Bradykinin inhibits the inflammation of tissues. Vasopressin controls blood pressure by regulating the contraction of smooth muscle. It is also an antidiuretic. Oxytocin induces labor in pregnant women and stimulates milk production in nursing mothers. Vasopressin and oxytocin both have an intrachain disulfide bond, and their C-terminal amino acids contain amide rather than carboxyl groups. Notice that the C-terminal amide group is indicated by writing NH2 after the name of the C-terminal amino acid. In spite of their very different physiological effects, vasopressin and oxytocin differ only by two amino acids. 

Oxytocin and vasopressin (Fig. 24.6) are two rather small polypeptides with strikingly similar structures (where oxytocin has leucine, vasopressin has arginine, and where oxytocin has isoleucine, vasopressin has phenylalanine). In spite of the similarity of their amino acid sequences, these two polypeptides have quite different physiological effects. Oxytocin occurs only in the female of a species and stimulates uterine contractions during childbirth. Vasopressin occurs in males and females it causes contraction of peripheral blood vessels... 

Oxytocin, a nine amino acid peptide, is synthesized primarily in the paraventricular and supraoptic (SON) nuclei of the hypothalamus, from which it is released to the general circulation through the posterior pituitary (Insel et ah, 1997). However, oxytocinergic fibers have also been found to project from the PVN to the limbic system and several autonomic centers in the brain stem. This central OT pool appears to be independent of pituitary OT release cerebrospinal fluid (CSF) and plasma OT responses to numerous stimuli are not correlated (Insel, 1997). Oxytocin and its analog (or partner) peptide vasopressin are found only in mammals. A related peptide, vasotocin, thought to be the evolutionary precedent of these peptides, is found in reptiles and birds. The first known actions of OT were its peripheral effects on the physiology of new mothers. In mammals, OT stimulates milk ejection and uterine contraction, essential aspects of maternal physiology (Insel et ah, 1997). 

Vasopressin occurs in two variations arginine-vasopressin (AVP) and lysine-vasopressin (LVP), in which Arg is replaced by Lys. The conformation of these hormones is almost identical to that of oxytocin, except that the terminal tail is con-formationally free and not held by the ring. The physiological role of the vasopressins is the regulation of water reabsorption in the renal tubules (i.e., an antidiuretic action). In high doses, they promote the contraction of arterioles and capillaries and an increase in blood pressure hence the name of these hormones. Because of their very similar structures, OT and VP overlap in a number of effects. 

In addition to its central effects on blood pressure, Ang II acts on the central nervous system to stimulate drinking (dipsogenic effect) and increase the secretion of vasopressin and adrenocorticotropic hormone (ACTH). The physiologic significance of the effects of Ang II on drinking and pituitary hormone secretion is not known. 

Vasopressin has a direct effect on the adrenal cortex at pharmacological doses, but it does not cause the release of ACTH at physiological concentrations. 

Vasopressin likely functions as a CNS neurotransmitter and/or neuromodulator but the physiological relevance of vasopressin s CNS effects is unclear Although vasopressin is not the principal corticotropin-releasing factor it may assist in sustained activation of the hypothalamic-pituitary-adrenal axis during chronic stress (see Chapter 59). CNS effects of vasopressin are mediated predominantly by V receptors. 

At high concentrations, vasopressin stimulates contraction of smooth muscle in the uterus ("via oxytocin receptors) and GI tract ("via V receptors). Vasopressin is stored in platelets, and activation of Vj receptors stimulates platelet aggregation. Also, activation of V receptors on hepato-cytes stimulates glycogenolysis. The physiological significance of these effects of vasopressin in not known. 

Therapeutic vasopressin infusion into the main arterial trunks induces visceral vasospasm, enhancing the physiological vasoconstrictive reaction against bleeding. Initial enthusiasm about vasopressin infusion ebbed away because of less favorable results compared to embolization [79-81], and the systemic side effects [82]. Vasopressin infusion has been shown more effective in lower than in upper GIH. 

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