Arginine vasopressin (AVP) is a neuropeptide mainly synthesized in the supraoptic and paraventricular nuclei in the hypothalamus and released from the posterior pituitary
when physiological demands are increased. The major function of circulating AVP is
to promote water retention and vasoconstriction, thereby maintaining hydromineral
homeostasis and blood volume and pressure. Physiological regulation of AVP
secretion includes osmotic and nonosmotic neurohumoral refexes, actions of blood-
borne factors, interactions between glia and AVP neurons, autoregulation, and other
cellular 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, efcient
arterial volume is relatively low despite water retention in the body; high levels of AVP
cannot correct insufciency of efcient arterial volume and/or high levels of circulating
renin-angiotensin-aldosterone. These nonosmotic factors can counterbalance and
even override the inhibitory efect of AVP-elicited hyponatremia on AVP secretion.
Under this condition, a facilitatory feature of local neural circuits controlling AVP
secretion becomes active, leading to further secretion of AVP. This inherent feature
in the local circuit mainly includes: 1) adaptive reduction of osmosensory threshold,
2) removal of astrocytic restriction of AVP neuronal activity, and 3) damaging efects
of protein tyrosine nitration on enzymes for glutamate conversion and on other
functional molecules. These factors will be discussed in this review.
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Título : Translational Biomedicine: Neurophysiological involvement in
hypervolemic hyponatremia-evoked by
hypersecretion of vasopressin
EAN : cdltb21720421
Editorial : Fundación de Neurociencias
Fecha de publicación
: 3/4/12
Formato : PDF
Tamaño del archivo : 1.43 mb
Protección : Adobe DRM
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hypervolemic hyponatremia-evoked by
hypersecretion of vasopressin está en formato PDF
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