Arginine vasopressin (AVP) is a neuropeptide mainly synthesized in the supraoptic andÂ paraventricular nuclei in the hypothalamus and released from the posterior pituitaryÂ when physiological demands are increased. The major function of circulating AVP isÂ to promote water retention and vasoconstriction, thereby maintaining hydromineralÂ homeostasis and blood volume and pressure. Physiological regulation of AVPÂ secretion includes osmotic and nonosmotic neurohumoral reflexes, actions of bloodborne factors, interactions between glia and AVP neurons, autoregulation, and otherÂ cellular events. These modulatory processes, ultimately integrated in AVP neurons,Â determine their firing rate and pattern and the amount of AVP secretion. In waterretaining diseases such as congestive heart failure and hepatic cirrhosis, efficientÂ arterial volume is relatively low despite water retention in the body; high levels of AVPÂ cannot correct insufficiency of efficient arterial volume and/or high levels of circulatingÂ renin-angiotensin-aldosterone. These nonosmotic factors can counterbalance andÂ even override the inhibitory effect of AVP-elicited hyponatremia on AVP secretion.Â Under Â this condition, a facilitatory feature of local Â neural circuits controlling AVPÂ secretion becomes active, leading to further secretion of AVP. This inherent featureÂ in the local circuit mainly includes: 1) adaptive reduction of osmosensory threshold,Â 2) removal of astrocytic restriction of AVP neuronal activity, and 3) damaging effectsÂ of protein tyrosine nitration on enzymes for glutamate conversion and on otherÂ functional molecules. These factors will be discussed in this review.
Yu-Feng Wang , Li-Xiao Liu , Hai-Peng Yang
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