POSSIBLE CONTRIBUTION OF POTASSIUM CHANNELS TO THE ENDOTHELIN-INDUCEDDILATATION OF RAT CORONARY VASCULAR BEDS

The mechanism for the endothelin (ET)-induced vasodilatation of the en dothelium-intact rat coronary vascular bed was investigated. Continuou s infusion (0.1-1 nM) or bolus injection (1-100 pmol) of ET-1 or ET-3 elicited a dose-related transient decrease, followed by a slight susta ined increase, in the coronary perfusion pressure (CPP). The decrease in CPP induced by an injection (10 pmol) of ET-1 or ET-3 was not modif ied by indomethacin (5 muM). However, oxyhemoglobin (5 mM) shortened t he duration of the ET-induced decrease in CPP, although it did not aff ect the magnitude. The ET-induced decrease in CPP was abolished by rai sing K+ in the perfusing solution from 5.9 to 16.9 mM. These findings suggest that the ET-induced dilatation of the rat coronary vascular be ds may not be mediated by cyclooxygenase products. The ET-induced vaso relaxation may be mediated, at least in part, by endothelium-derived r elaxing factor and may be related to opening of K+ channels.