File(s) under permanent embargo

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

journal contribution
posted on 2008-11-01, 00:00 authored by Brett Jennings, John DonaldJohn Donald
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.



American journal of physiology : regulatory, integrative and comparative physiology






1640 - 1646


American Physiological Society


Bethesda, Md.







Publication classification

C1 Refereed article in a scholarly journal

Copyright notice

2008, American Physiological Society