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Adenosine and hypoxic dilation of rat coronary small arteries: roles of the ATP-sensitive potassium channel, endothelium, and nitric oxide

Cardiovascular Research Group, Department of Medicine, Manchester Royal Infirmary, Manchester, United Kingdom

Submitted 30 March 2005 ; accepted in final form 13 October 2005

The aims of the study were to examine the roles of the ATP-sensitive potassium (K_ATP) channel, the endothelium, and nitric oxide (NO) in the responses of rat coronary small arteries to adenosine and hypoxia. Segments of rat coronary vessel were investigated in vitro using pressure myography; all vessels studied developed stable spontaneous myogenic tone during equilibration. Glibenclamide (a K_ATP channel inhibitor) reversed pinacidil but not 2-deoxyglucose-induced dilation. Both adenosine and hypoxia dilated the vessels, and glibenclamide did not reverse these responses. Endothelial removal or N^G-nitro-L-arginine methyl ester (L-NAME) inhibited the dilation to adenosine by 50%; subsequent addition of glibenclamide was without effect. Hypoxic dilation was completely inhibited by endothelium removal or L-NAME. We conclude that adenosine- and hypoxia-induced dilation of rat coronary arteries does not appear to involve the K_ATP channel. Adenosine-induced dilation is partially and hypoxic dilation is completely dependent on endothelium-derived NO.

myogenic tone; hypoxia

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				K. M. Gauthier Hypoxia-induced vascular smooth muscle relaxation: increased ATP-sensitive K+ efflux or decreased voltage-sensitive Ca2+ influx? Am J Physiol Heart Circ Physiol, July 1, 2006; 291(1): H24 - H25. [Full Text] [PDF]