TRANSLATIONAL BIOMEDICINE: NEUROPHYSIOLOGICAL INVOLVEMENT INHYPERVOLEMIC HYPONATREMIA-EVOKED BYHYPERSECRETION OF VASOPRESSIN by VV. AA.

Synopsis

TRANSLATIONAL BIOMEDICINE: NEUROPHYSIOLOGICAL INVOLVEMENT INHYPERVOLEMIC HYPONATREMIA-EVOKED BYHYPERSECRETION OF VASOPRESSIN

Arginine vasopressin (AVP) is a neuropeptide mainly synthesized in the supraoptic and paraventricular nuclei in the hypothalamus and released from the posterior pituitarywhen physiological demands are increased.

The major function of circulating AVP isto promote water retention and vasoconstriction, thereby maintaining hydromineralhomeostasis and blood volume and pressure. Physiological regulation of AVPsecretion includes osmotic and nonosmotic neurohumoral refexes, actions of blood-borne factors, interactions between glia and AVP neurons, autoregulation, and othercellular events.

These modulatory processes, ultimately integrated in AVP neurons,determine their fring rate and pattern and the amount of AVP secretion. In water-retaining diseases such as congestive heart failure and hepatic cirrhosis, efcientarterial volume is relatively low despite water retention in the body; high levels of AVPcannot correct insufciency of efcient arterial volume and/or high levels of circulatingrenin-angiotensin-aldosterone. These nonosmotic factors can counterbalance andeven override the inhibitory efect of AVP-elicited hyponatremia on AVP secretion.Under this condition, a facilitatory feature of local neural circuits controlling AVPsecretion becomes active, leading to further secretion of AVP.

This inherent featurein the local circuit mainly includes: 1) adaptive reduction of osmosensory threshold,2) removal of astrocytic restriction of AVP neuronal activity, and 3) damaging efectsof protein tyrosine nitration on enzymes for glutamate conversion and on otherfunctional molecules.

These factors will be discussed in this review.

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