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

The effect of reduced Po-2 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 mu m ID) were cannulated with glass micropipettes and perfused and superfused with physiological salt solution. Lowering the Po-2 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 mu M). However, low Po-2 did not significantly dilate either endothelium-intact or -denuded coronary resistance arteries, although superfusion with 1 mu M cromakalim, a K+-channel activator, induced a 6-mV hyperpolarization and increased the diameter by 33 +/- 10 mu m These results suggest that reduced Po-2 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 Po-2.