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2-Deoxyglucose-induced vasodilation and hyperpolarization in rat coronary artery are reversed by glibenclamide.
Conway M, Nelson MT, Brayden J
American Journal of Physiology-Heart and Circulatory Physiology. 1994;266( 4 Pt 2):H1322-6.
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Abstract
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.
Keyword(s)
Animals; Cromakalim; Dose-Response Relationship, Drug; Electrophysiology; Female; Male; Potassium Channel Blockers; Rats; Rats, Sprague-Dawley; Vasodilation; drug effects: Coronary Vessels; pharmacology: Benzopyrans; pharmacology: Deoxyglucose; pharmacology: Glyburide; pharmacology: Pyrroles