2-DEOXYGLUCOSE-INDUCED VASODILATION AND HYPERPOLARIZATION IN RAT CORONARY-ARTERY ARE REVERSED BY GLIBENCLAMIDE

The mechanisms responsible for coronary vasodilation during ischemia or hypoxia are poorly understood. It has recently been suggested that alterations in intracellular ATP may play a role in this response. We examined whether dilation of isolated coronary arteries in response to metabolic blockade by 2-deoxyglucose, which competitively inhibits glycolysis and glycogenolysis, was sensitive to glibenclamide, an inhibitor of ATP-sensitive potassium channels. Pressurized rat coronary arteries with myogenic tone dilated in response to 2-deoxyglucose by an endothelium-independent mechanism. The dilation was accompanied by a substantial hyperpolarization. Addition of glibenclamide partially reversed this vasodilation and abolished the hyperpolarization. We propose that ATP-sensitive potassium channels play a significant role in the dilator response to 2-deoxyglucose. This may have implications both for ischemia-induced coronary vasodilation and for the use of oral hypoglycemic agents in general.