Hypoxia-induced hyperpolarization is not associated with
vasodilation of bovine coronary resistance arteries.
Gauthier-Rein, Kathryn M., Donna M. Bizub, Julian H. Lombard, and
Nancy J. Rusch.
Department of Physiology, Medical College of Wisconsin, Milwaukee,
WI 53226
APStracts 3:0443H, 1996.
The effect of reduced pO2 on transmembrane potential (Em) and diameter
of small cannulated coronary resistance arteries (CRA) was evaluated
by microelectrode and videomicroscopy methods. Bovine CRA (i.d. = 158
+/- 8 [mu]m) were cannulated with glass micropipettes, and perfused
and superfused with physiological salt solution (PSS). Lowering the
partial pressure of oxygen of the PSS from 140 +/- 4 mm Hg to 36 +/-
2 mm Hg increased smooth muscle cell Em from -51 +/- 2 mV to -62 +/-
2 mV in both endothelium-intact and denuded CRA. This
hyperpolarization was blocked by superfusion with the K+ channel
blocker glibenclamide (1 [mu]M). However low pO2 did not
significantly dilate either endothelium-intact or denuded CRA,
although superfusion with 1 [mu]M cromakalim, a K+ channel activator,
induced a 6 mV hyperpolarization and increased diameter by 33 +/- 10
[mu]m. These results suggest that reduced pO2 directly hyperpolarizes
vascular smooth muscle of CRA by activation of glibenclamide
-sensitive K+ channels, but other nonvascular mechanisms may mediate
the vasodilation response to low pO2.
Received 20 February 1996; accepted in final form 11 October
1996.
APS Manuscript Number H166-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996