Mechanisms involved in coronary artery dilatation during respiratory acidosis in the isolated perfused rat heart.
A rat Langendorff heart preparation, perfused at constant pressure, was used to evaluate the role of K(ATP) channels in respiratory acidosis-induced coronary hyperemia. Prior administration of glibenclamide, an inhibitor of K(ATP) channels, reduced basal flow rates and eliminated the hyperemia associated with hypercapnia. These results implicate K(ATP) channels as a functional link in the respiratory acidosis-induced increase in coronary flow.
Phillis
J W
JW
Department of Physiology, Wayne State University, Detroit, MI 48201, USA. jpillis@med.wayne.edu
Song
D
D
O'Regan
M H
MH
D000142:Acidosis, Respiratory / Q000503:physiopathology*; D000818:Animals; D002245:Carbon Dioxide / Q000494:pharmacology; D003326:Coronary Circulation; D019204:GTP-Binding Proteins / Q000502:physiology; D005905:Glyburide / Q000494:pharmacology; D006940:Hyperemia / Q000209:etiology; D008297:Male; D010477:Perfusion; D015221:Potassium Channels / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D014664:Vasodilation
D015221:Potassium Channels; D002245:Carbon Dioxide; D019204:GTP-Binding Proteins; D005905:Glyburide