Vasopressin physiology

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). 

Indicate the source, factors regulating the release, and physiological significance of the following vasoconstrictors catecholamines, angiotensin II, vasopressin, endothelin, and thromboxane A2... 

In order to make adjustments in the water load, the reabsorption of the remaining 20% of the filtered water from the distal tubule and the collecting duct is physiologically controlled by antidiuretic hormone (ADH), also referred to as vasopressin. Antidiuretic hormone, synthesized in the hypothalamus and released from the neurohypophysis of the pituitary gland, promotes the... 

Diabetes insipidus occurs with a loss of vasopressin production in the Brattleboro rat model 330 Mutations and knockouts of peptide-processing enzyme genes cause a myriad of physiological problems 330 Neuropeptides play key roles in appetite regulation and obesity 330 Enkephalin knockout mice reach adulthood and are healthy 331 Neuropeptides are crucial to pain perception 331... 

Taylor The voltage clamp is more useful than measuring currents. Nonetheless, a cell that is responding to vasopressin is not voltage clamped in a physiological situation. 

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 (antidiuretic hormone, ADH) plays an important role in the long-term control of blood pressure through its action on the kidney to increase water reabsorption. This and other aspects of the physiology of vasopressin are discussed in Chapters 15 and 37 and will not be reviewed here. 

Maybauer MO et al Physiology of the vasopressin receptors. Best Pract Res Clin Anaesthesiol 2008 22 253. [PMID 18683472]... 

Polydipsia and polyuria are common but reversible concomitants of lithium treatment, occurring at therapeutic serum concentrations. The principal physiologic lesion involved is loss of responsiveness to antidiuretic hormone (nephrogenic diabetes insipidus). Lithium-induced diabetes insipidus is resistant to vasopressin but responds to amiloride. 

In the absence of physiologic amounts of cortisol, renal function (particularly glomerular filtration) is impaired, vasopressin secretion is augmented, and there is an inability to excrete a water load normally. 

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