The aims of the study were to examine the roles of the ATP-sensitive potassium channel (K_ATP), 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; during equilibration all vessels included developed stable spontaneous myogenic tone. 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 inhibit these responses. Endothelial removal or L-NAME inhibited the dilation to adenosine by approximately 50%; subsequent addition of glibenclamide was without effect. Hypoxic dilation was completely inhibited by endothelial removal or L-NAME. We conclude that adenosine and hypoxia induced dilation of rat coronary arteries does not appear to involve K_ATP. Adenosine induced dilation is partially, and hypoxic dilation is completely dependent on endothelial derived NO.