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• W1989559838 abstract "We tested a number of hypotheses concerning the mechanism of K+-induced vasodilation of the coronary vascular bed. Blood flow in the circumflex artery was measured in pentobarbital-anesthetized, open-chest dogs. Intracircumflex artery bolus injections of 40 mumol of isomotic KCl produced decreases in coronary vascular resistance ranging from 34% to 48%, depending on the initial resistance of the vascular bed. K+ administration had no effect on heart rate and produced a 4 mm Hg decrease in mean arterial pressure. K+ injection caused a 0.2 vol% increase in coronary sinus O2 content in a preparation in which left common coronary flow was held constant. The magnitude of K+-induced vasodilation was not significantly affected by the administration of propranolol, atropine, phentolamine, or lidocaine. K+-induced vasodilation was attenuated (50%) by ouabain plus lidocaine. Acetylcholine-induced vasodilation was not significantly diminished by ouabain plus lidocaine. We conclude that the mechanism of K+-induced vasodilation does not involve an increase in the metabolic activity of the heart or an interaction between K+ and tissue neural elements. Our data do support the hypothesis that K+-induced vasodilation is at least partly the result of an activation of the electrogenic Na+-K+ transport system of coronary smooth muscle." @default.
• W1989559838 created "2016-06-24" @default.
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• W1989559838 date "1978-01-01" @default.
• W1989559838 modified "2023-09-25" @default.
• W1989559838 title "The mechanism of K+-induced vasodilation of the coronary vascular bed of the dog." @default.
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• W1989559838 doi "https://doi.org/10.1161/01.res.42.1.35" @default.
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