Affiliations: [a] The First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, 980, Japan | [b] The Department of Internal Medicine and the Cardiovascular Center, College of Medicine, University of Iowa, Iowa City, IA 52242, USA
Abstract: The ATP-sensitive potassium channel (K+ATP channel) is known to exist in blood vessels and to regulate vascular tone. We examined the role of this channel in coronary arteriolar vasomotion during coronary autoregulation, ischemia, reactive hyperemia and endothelium-dependent response by acetylcholine in vivo. Experiments were performed with anesthetized open-chest dogs. Coronary arterioles were directly observed in situ by means of a floating objective system or a stroboscropic epi-illumination system synchronized with cardiac motion. Small arterioles less than 100 μm in internal diameter dilated in response to reduction in perfusion pressure (perfusion pressure: 60, 40, 25 mm Hg). Glibenclamide, a selective blocker of the K+ATP channel, reversed the dilation. Reactive hyperemia produced by 20-second occlusion of the left anterior descending coronary artery resulted in arteriolar dilation, the magnitude of which was greater in smaller arterioles than in larger ones. Glibenclamide significantly inhibited the dilation in both large and small arterioles. Acetylcholine (ACh) produced dilation in arterioles of all sizes. NG-monomethyl L-arginine, a competitive inhibitor of nitric oxide synthesis, abolished the dilation of large arterioles, but failed to abolish the dilation in small arterioles. Glibenclamide, however, did not have any additional inhibitory effect on ACh-induced arteriolar dilation. Thus, we conclude that the K+ATP channel plays an important role in coronary microvascular vasomotion during autoregulation, ischemia and reactive hyperemia, but not during endothelium-dependent vasodilation induced by ACh in vivo.
