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Neurally-derived nitric oxide regulates vascular tone in pulmonary and cutaneous arteries of the toad, Bufo marinus

Jennings, Brett L. and Donald, John A. 2008, Neurally-derived nitric oxide regulates vascular tone in pulmonary and cutaneous arteries of the toad, Bufo marinus, American journal of physiology : regulatory, integrative and comparative physiology, vol. 295, no. 5, pp. 1640-1646, doi: 10.1152/ajpregu.00057.2008.

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Title Neurally-derived nitric oxide regulates vascular tone in pulmonary and cutaneous arteries of the toad, Bufo marinus
Formatted title Neurally-derived nitric oxide regulates vascular tone in pulmonary and cutaneous arteries of the toad, Bufo marinus
Author(s) Jennings, Brett L.
Donald, John A.ORCID iD for Donald, John A. orcid.org/0000-0001-5930-2642
Journal name American journal of physiology : regulatory, integrative and comparative physiology
Volume number 295
Issue number 5
Start page 1640
End page 1646
Total pages 7
Publisher American Physiological Society
Place of publication Bethesda, Md.
Publication date 2008-11
ISSN 0363-6119
1522-1490
Keyword(s) endothelium
nitric oxide synthase
autonomic nervous system
amphibian
vasodilation
Summary In this study, the role of nitric oxide (NO) in regulation of the pulmocutaneous vasculature of the toad, Bufo marinus was investigated. In vitro myography demonstrated the presence of a neural NO signaling mechanism in both arteries. Vasodilation induced by nicotine was inhibited by the soluble guanylyl cyclase (GC) inhibitor, 1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one, and the NO synthase (NOS) inhibitor, Nω-nitro-L-arginine (L-NNA). Removal of the endothelium had no significant effect on the vasodilation. Furthermore, pretreatment with N5-(1-imino-3-butenyl)-L-ornithine (vinyl-L-NIO), a more specific inhibitor of neural NOS, caused a significant decrease in the nicotine-induced dilation. In the pulmonary artery only, a combination of L-NNA and the calcitonin gene-related peptide (CGRP) receptor antagonist, CGRP(8-37), completely blocked the nicotine-induced dilation. In both arteries, the vasodilation was also significantly decreased by glibenclamide, an ATP-sensitive K+ (K+ATP) channel inhibitor. Levcromakalim, a K+ATP channel opener, caused a dilation that was blocked by glibenclamide in both arteries. In the pulmonary artery, NO donor-mediated dilation was significantly decreased by pretreatment with glibenclamide. The physiological data were supported by NADPH-diaphorase histochemistry and immunohistochemistry, which demonstrated NOS in perivascular nerve fibers but not the endothelium of the arteries. These results indicate that the pulmonary and cutaneous arteries of B. marinus are regulated by NO from nitrergic nerves rather than NO released from the endothelium. The nitrergic vasodilation in the arteries appears to be caused, in part, via activation of K+ATP channels. Thus, NO could play an important role in determining pulmocutaneous blood flow and the magnitude of cardiac shunting.
Language eng
DOI 10.1152/ajpregu.00057.2008
Field of Research 060603 Animal Physiology - Systems
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1 Refereed article in a scholarly journal
HERDC collection year 2008
Copyright notice ©2008, American Physiological Society
Persistent URL http://hdl.handle.net/10536/DRO/DU:30017737

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