Inhibition of adenosine-activated k+ current by glybenclamide in
guinea pig atrial myocytes is not due to specific blockade of katp
channels.
Song, Yejia, Miduturu Srinivas, Luiz Belardinelli.
Departments of Medicine and Pharmacology, University of Florida,
Gainesville, FL 32610
APStracts 3:0208H, 1996.
The ATP-sensitive K+ (KATP) channel blocker, glybenclamide, was
reported to inhibit the K+ current activated by adenosine. This study
investigated whether the inhibition by glybenclamide of adenosine
-induced current is due to a specific blockade of KATP channels in
guinea pig atrial myocytes. In the absence of adenosine, the basal
background current was an inward rectifier K+ current (IK1).
Glybenclamide at concentrations of 10, 30 and 100 [mu]M reduced the
basal background K+ current by 15+/-6%, 43+/-10% and 63+/-11%,
respectively. In the presence of adenosine (10 [mu]M), glybenclamide
(30 [mu]M) decreased the adenosine-induced K+ current by 39+/-3%. A
similar inhibitory effect of glybenclamide on the outward K+ currents
activated by either the muscarinic agonist carbachol or the non
-hydrolyzable GTP analogue GTP_S was observed. A low concentration (1
[mu]M) of glybenclamide did not significantly attenuate the current
elicited by adenosine, although it completely abolished the outward
K+ current activated by pinacidil, a KATP channel opener. Thus we
conclude that the inhibition of adenosine-induced K+ current by
glybenclamide at high concentrations (> 1 [mu]M) is not due to a
specific blockade of KATP channels, but rather, resulted from a
blockade of IK1.
Received 12 February 1996; accepted in final form 6 May 1996.
APS Manuscript Number H140-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 19 May 96