Maintained Vasodilatory Response to Cromakalim After Inhibition of Nitric Oxide Synthesis

Activation of vascular smooth-muscle adenosine triphosphate-sensitive potassium channels (KATP channels) causes membrane hyperpolarization, reduced entry of Ca through L-type voltage-gated Ca channels, and subsequent smooth-muscle relaxation. Conversely, opening of endothelial KATP channels elicits...

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Published in:	Journal of cardiovascular pharmacology Vol. 31; no. 6; pp. 921 - 929
Main Authors:	Herrera, Gerald M, Resta, Thomas C, Candelaria, John J, Walker, Benjimen R
Format:	Journal Article
Language:	English
Published:	Philadelphia, PA Lippincott-Raven Publishers 01-06-1998 Hagerstown, MD Lippincott
Subjects:	Animals Arteries - drug effects Biological and medical sciences Blood vessels and receptors Calcium - metabolism Cells, Cultured Cromakalim - pharmacology Endothelium, Vascular - cytology Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Fundamental and applied biological sciences. Psychology Male Nitric Oxide - antagonists & inhibitors Nitric Oxide - biosynthesis Rats Rats, Sprague-Dawley Tail - blood supply Vasodilator Agents - pharmacology Vertebrates: cardiovascular system Cell culture Endothelial cell Rat Lung Rodentia Ionic channel In vitro Pulmonary artery Artery Vasodilation Potassium channel agonist Endothelium In vivo Vertebrata Mammalia Calcium ion Cromakalim Animal Nitric oxide Blood vessel Tail Circulatory system Intracellular Potassium
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Summary:	Activation of vascular smooth-muscle adenosine triphosphate-sensitive potassium channels (KATP channels) causes membrane hyperpolarization, reduced entry of Ca through L-type voltage-gated Ca channels, and subsequent smooth-muscle relaxation. Conversely, opening of endothelial KATP channels elicits hyperpolarization but may induce Ca influx and stimulation of endothelium-derived nitric oxide (EDNO) because these cells appear not to possess L-type Ca channels. We therefore hypothesized that EDNO contributes to KATP channel-mediated vasodilation. To test this hypothesis, we examined vasodilatory responses to the KATP channel opener cromakalim in conscious rats, perfused rat tail artery segments, and isolated perfused rat lungs in the presence or absence of the EDNO synthesis inhibitor N-nitro-L-arginine (L-NNA). Additionally, we compared the effect of cromakalim with the EDNO-dependent dilator bradykinin on NO production and intracellular Ca in cultured rat pulmonary artery endothelial cells. Vasodilatory profiles to cromakalim were unaffected by L-NNA in conscious rats, tail arteries, and isolated lungs. Consistent with these results, cromakalim had no apparent effect on either NO synthesis or Ca levels in cultured endothelial cells. These data suggest a lack of a role for EDNO in contributing to KATP-channel-mediated vasodilation in the rat.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0160-2446 1533-4023
DOI:	10.1097/00005344-199806000-00017