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AJP - Heart and Circulatory Physiology, Vol 272, Issue 1 325-H333, Copyright © 1997 by American Physiological Society
ARTICLES |
E. Kim, J. Han, W. Ho and Y. E. Earm
Department of Physiology and Biophysics, College of Medicine, Inje Universty, Pusan, Korea.
The objective of the present study was to characterize the role of adenosine in the regulation of ATP-sensitive K (KATP) channel activity in isolated rabbit ventricular myocytes using the patch-clamp technique. In an outside-out patch exposed to guanosine 5'-triphosphate and ATP at the intracellular surface, external adenosine stimulated KATP channel activity. In an inside-out patch exposed to external adenosine, ATP reduced KATP channel activity and guanosine 5'-triphosphate stimulated KATP channel activity. Guanosine 5'-O-(3-thiotriphosphate) resulted in a gradual increase of KATP channel activity even in the absence of adenosine. When myocytes were preincubated with pertussis toxin or 8-cyclopentyl-1,3-dipropylxanthine, adenosine A1 receptor activation failed to activate the KATP channel. Analysis of the open and closed time distributions showed that adenosine A1 receptor activation increased burst duration and decreased interburst duration. In a dose-response relationship for ATP, adenosine A1 receptor activation shifted the half-maximal inhibition of the KATP channel from 70 to 241 microM.
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