Role of neuronal nitric oxide in the regulation of vasopressin expression and release in response to inhibition of cathecholamine synthesis and dehydration
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Date
2007-10-22
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Authors
Yamova, Liubov
Atochin, Dmitriy
Glazova, Margarita
Chernigovskaya, Elena
Huang, Paul
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East Carolina University
Abstract
We used neuronal nitric oxide synthase (nNOS) gene knockout mice to study the effects of
catecholamines and neuronal nitric oxide on vasopressin expression in the hypothalamic
neurosecretory centers. nNOS gene deletion did not change the level of vasopressin mRNA in the
supraoptic or paraventricular nuclei. In contrast, vasopressin immunoreactivity was lower in nNOS
deficient mice than in wild-type animals. Dehydration increased vasopressin mRNA levels and
decreased vasopressin immunoreactivity in both wild-type and nNOS knockout mice, but these
responses were more marked in the nNOS knockout mice. Treatment with α-mpt, a pharmacologic
inhibitor of catecholamine synthesis, resulted in increased vasopressin mRNA levels in wild-type
mice and in reduced vasopressin immunoreactivity in both wild-type and nNOS knockout mice. From
these results, we conclude: (1) neuronal nitric oxide suppresses vasopressin expression under basal
conditions and during activation of the vasopressin-ergic system by dehydration; (2) catecholamines
limit vasopressin expression; (3) nNOS is required for the effects of catecholamines on vasopressin
expression. Originally published Neuroscience Letters, Vol. 426, No. 3, Oct 2007
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Neuroscience Letters; 426:3 p. 160-165