Mechanisms involved in coronary artery dilatation during respiratory acidosis in the isolated perfused rat heart

Abstract

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.