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

Jennings, Brett L. and Donald, John A. 2010, Mechanisms of nitric oxide-mediated neurogenic,vasodilation in mesenteric resistance arteries of toad, Bufo marinus, American journal of physiology regulatory intergrative and comparative physiology, vol. 298, no. 3, pp. R767-R775.

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Title Mechanisms of nitric oxide-mediated neurogenic,vasodilation in mesenteric resistance arteries of toad, Bufo marinus
Formatted title Mechanisms of nitric oxide-mediated neurogenic,vasodilation in mesenteric resistance arteries of toad, Bufo marinus
Author(s) Jennings, Brett L.
Donald, John A.
Journal name American journal of physiology regulatory intergrative and comparative physiology
Volume number 298
Issue number 3
Start page R767
End page R775
Total pages 9
Publisher American Physiological Society
Place of publication Bethesda, Md.
Publication date 2010-03-01
ISSN 0363-6119
1522-1490
Keyword(s) amphibian
autonomic nervous system
nitric oxide synthase
endothelium
Summary 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.
Notes First published January 13, 2010
Language eng
Field of Research 111603 Systems Physiology
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1 Refereed article in a scholarly journal
HERDC collection year 2010
Copyright notice ©2010, American Physiological Society
Persistent URL http://hdl.handle.net/10536/DRO/DU:30032912

Document type: Journal Article
Collection: School of Life and Environmental Sciences
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