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Mechanisms of nitric oxide-mediated neurogenic,vasodilation in mesenteric resistance arteries of toad, Bufo marinus

journal contribution
posted on 2010-03-01, 00:00 authored by Brett Jennings, John DonaldJohn Donald
This study determined the role of nitric oxide (NO) in neurogenic vasodilation in mesenteric resistance arteries of the toad Bufo marinus. NO synthase (NOS) was anatomically demonstrated in perivascular nerves, but not in the endothelium. ACh and nicotine caused TTX-sensitive neurogenic vasodilation of mesenteric arteries. The ACh-induced vasodilation was endothelium-independent and was mediated by the NO/soluble guanylyl cyclase signaling pathway, inasmuch as the vasodilation was blocked by the soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one and the NOS inhibitors Nω- nitro-L-arginine methyl ester and Nω-nitro-L-arginine. Furthermore, the ACh-induced vasodilation was significantly decreased by the more selective neural NOS inhibitor N5-(1-imino-3-butenyl)-L-ornithine. The nicotine-induced vasodilation was endothelium-independent and mediated by NO and calcitonin gene-related peptide (CGRP), inasmuch as pretreatment of mesenteric arteries with a combination of Nω-nitro-L-arginine and the CGRP receptor antagonist CGRP-(8–37) blocked the vasodilation. Clotrimazole significantly decreased the ACh-induced response, providing evidence that a component of the NO vasodilation involved Ca2+-activated K+ or voltage-gated K+ channels. These data show that NO control of mesenteric resistance arteries of toad is provided by nitrergic nerves, rather than the endothelium, and implicate NO as a potentially important regulator of gut blood flow and peripheral blood pressure.

History

Journal

American journal of physiology regulatory intergrative and comparative physiology

Volume

298

Issue

3

Publisher

American Physiological Society

Location

Bethesda, Md.

ISSN

0363-6119

eISSN

1522-1490

Language

eng

Notes

First published January 13, 2010

Publication classification

C1 Refereed article in a scholarly journal

Copyright notice

2010, American Physiological Society