Hypoxia-induced hyperpolarization is not associated with vasodilation of bovine coronary resistance arteries

The effect of reduced PO2 on the transmembrane potential and diameter of small cannulated coronary resistance arteries was evaluated by microelectrode and videomicroscopic methods. Bovine coronary resistance arteries (158 +/- 8 microm ID) were cannulated with glass micropipettes and perfused and sup...

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Published inThe American journal of physiology Vol. 272; no. 3 Pt 2; p. H1462
Main Authors Gauthier-Rein, K M, Bizub, D M, Lombard, J H, Rusch, N J
Format Journal Article
LanguageEnglish
Published United States 01.03.1997
Subjects
Acetylcholine - pharmacology
Animals
Benzopyrans - pharmacology
Bradykinin - pharmacology
Calcium - pharmacology
Cattle
Coronary Vessels - drug effects
Coronary Vessels - physiology
Cromakalim
Endothelium, Vascular - physiology
Glyburide - pharmacology
Hypoxia
In Vitro Techniques
Membrane Potentials
Microelectrodes
Microscopy, Video
Oxygen - blood
Perfusion
Pyrroles - pharmacology
Vascular Resistance - drug effects
Vasodilation - drug effects
Vasodilator Agents - pharmacology
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Summary:The effect of reduced PO2 on the transmembrane potential and diameter of small cannulated coronary resistance arteries was evaluated by microelectrode and videomicroscopic methods. Bovine coronary resistance arteries (158 +/- 8 microm ID) were cannulated with glass micropipettes and perfused and superfused with physiological salt solution. Lowering the PO2 of the physiological salt solution from 140 +/- 4 to 36 +/- 2 mmHg increased the smooth muscle cell transmembrane potential from -51 +/- 2 to -62 +/- 2 mV in both endothelium-intact and -denuded coronary resistance arteries. This hyperpolarization was blocked by superfusion with the K+-channel blocker glibenclamide (1 microM). However, low PO2 did not significantly dilate either endothelium-intact or -denuded coronary resistance arteries, although superfusion with 1 microM cromakalim, a K+-channel activator, induced a 6-mV hyperpolarization and increased the diameter by 33 +/- 10 microm. These results suggest that reduced PO2 directly hyperpolarizes the vascular smooth muscle of coronary resistance arteries by activation of glibenclamide-sensitive K+ channels, but other nonvascular mechanisms may mediate the vasodilation response to low PO2.
ISSN:0002-9513
DOI:10.1152/ajpheart.1997.272.3.h1462