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 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.