Functional hyperemia in striated muscle is reduced following
blockade of atp-sensitive potassium channels.
Saito, Yuichiro, Mary McKay, Akin Eraslan, and Robert L. Hester.
Department of Physiology and Biophysics, University of Mississippi
Medical Center, 2500 North State Street, Jackson, MS 39216-4505
APStracts 2:0467H, 1995.
This study was designed to determine the role of adenosine
triphosphate (ATP)-sensitive potassium channels in the control of the
arteriolar diameter during functional hyperemia. The hamster
cremaster muscle was prepared for in vivo microscopy and stimulated
electrically for one minute before and after topical application of
10 [mu]M glibenclamide to block ATP-sensitive potassium channels.
Glibenclamide treatment resulted in a small, though not significant,
decrease in resting arteriolar diameter (p>0.05). Glibenclamide
almost completely inhibited the vasodilation of the first-order and
the third-order arterioles in response to topical application of 1
[mu]M cromakalim (p<0.05). During muscle stimulation, the first
-order arterioles dilated from 69+/-3 to 89+/-3 [mu]m (n=7) and the
third-order arterioles dilated from 16+/-1 to 35+/-2 [mu]m (n=7). In
this set of experiments glibenclamide treatment resulted in a
significant decrease, 4 [mu]m, in the resting diameters of the first
-order arterioles, but had no significant effect on the resting
diameter of third-order arterioles. Glibenclamide treatment
significantly attenuated the vasodilation associated with muscle
contraction to 72+/-3 [mu]m, and to 21+/-3 [mu]m, respectively
(p<0.05). These results suggest that ATP-sensitive potassium
channels are an important mediator in the vasodilatory response to
muscle stimulation in the hamster cremaster muscle.
Received 21 June 1995; accepted in final form 2 October 1995.
APS Manuscript Number H564-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95