Role of neuronal nitric oxide in the regulation of vasopressin expression and release in response to inhibition of cathecholamine synthesis and dehydration

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)

Dmitriy Atochin (Creator)

Elena Chernigovskaya (Creator)

Margarita Glazova (Creator)

Paul Huang (Creator)

Liubov Yamova (Creator)

Institution

East Carolina University (ECU )

Web Site: http://www.ecu.edu/lib/

Abstract: We used neuronal nitric oxide synthase (nNOS) gene knockout mice to study the effects of atecholamines and neuronal nitric oxide on vasopressin expression in the hypothalamic eurosecretory centers. nNOS gene deletion did not change the level of vasopressin mRNA in the upraoptic or paraventricular nuclei. In contrast vasopressin immunoreactivity was lower in nNOS eficient mice than in wild-type animals. Dehydration increased vasopressin mRNA levels and ecreased vasopressin immunoreactivity in both wild-type and nNOS knockout mice but these esponses were more marked in the nNOS knockout mice. Treatment with α-mpt a pharmacologic nhibitor of catecholamine synthesis resulted in increased vasopressin mRNA levels in wild-type ice and in reduced vasopressin immunoreactivity in both wild-type and nNOS knockout mice. From hese results we conclude: (1) neuronal nitric oxide suppresses vasopressin expression under basal onditions and during activation of the vasopressin-ergic system by dehydration; (2) catecholamines imit vasopressin expression; (3) nNOS is required for the effects of catecholamines on vasopressin xpression. Originally published Neuroscience Letters Vol. 426 No. 3 Oct 2007

Additional Information

Publication

Other

Neuroscience Letters. 426:3(October 2007) p. 160-165.

Language: English

Date: 2011

Keywords

vasopressin, Nitric Oxide, catecholamines

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