Possible contribution of potassium channels to the endothelin-induced dilatation of rat coronary vascular beds.
The mechanism for the endothelin (ET)-induced vasodilatation of the endothelium-intact rat coronary vascular bed was investigated. Continuous 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 sustained 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 modified by indomethacin (5 microM). However, oxyhemoglobin (5 mM) shortened the duration of the ET-induced decrease in CPP, although it did not affect the magnitude. The ET-induced decrease in CPP was abolished by raising 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 beds may not be mediated by cyclooxygenase products. The ET-induced vasorelaxation may be mediated, at least in part, by endothelium-derived relaxing factor and may be related to opening of K+ channels.
Sakuma
I
I
Department of Cardiovascular Medicine, School of Medicine, Hokkaido University, Sapporo, Japan.
Asajima
H
H
Fukao
M
M
Tohse
N
N
Tamura
M
M
Kitabatake
A
A
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects*; D003331:Coronary Vessels / Q000187:drug effects; D016232:Endothelins / Q000494:pharmacology*; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D009569:Nitric Oxide / Q000494:pharmacology; D010108:Oxyhemoglobins / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D014664:Vasodilation / Q000187:drug effects*
D016232:Endothelins; D010108:Oxyhemoglobins; D015221:Potassium Channels; D009569:Nitric Oxide; D011188:Potassium; D007213:Indomethacin