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Eur J Pharmacol. 2005 Dec 28;528(1-3):144-9.

Role of voltage-sensitive calcium-channels in nitric oxide-mediated vasodilation in spontaneously hypertensive rats.

Author information

1
Department of Pharmacology and Physiology, University of Georgia, Athens, GA 30602-7389, USA. slewis@vet.uga.edu

Abstract

This study demonstrates that the vasodilator potencies of nitric oxide (NO) donors such as sodium nitroprusside are increased in conscious Spontaneously Hypertensive (SH) as compared to Wistar Kyoto (WKY) rats. For example, the NO donors do not dilate hindlimb resistance arteries in WKY rats whereas they elicit pronounced vasodilator responses in SH rats. This study also demonstrates that the NO-mediated vasodilator responses in WKY and SH rats were markedly diminished after blockade of voltage-sensitive Ca2+-channels (CaVS2+-channels) with nifedipine, diltiazem or verapamil. These findings suggest that NO dilates resistance arteries in vivo via direct and/or hyperpolarization-induced closure of CaVS2+-channels and that the increased potency of NO in SH rats may be due to the augmented CaVS2+-channel activity reported in this strain.

PMID:
16321377
DOI:
10.1016/j.ejphar.2005.10.056
[Indexed for MEDLINE]

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