OBJECTIVE: The aim was to study the effects, mode of action, and binding sites of endothelin-1 in the human uterine artery. STUDY DESIGN: The contractile effect of endothelin-1 on the human uterine artery with and without endothelium and the effect of verapamil and nicardipine on the contraction was investigated in vitro. The Student t test was used. Iodine 125-endothelin-1 binding sites were localized with autoradiography. RESULTS: Endothelin-1 induced a contraction that was unaffected by removal of the endothelium. Verapamil antagonized the contraction, whereas nicardipine showed no effect. Iodine 125-endothelin-1 binding sites were demonstrated in the smooth muscle layer. CONCLUSIONS: These results show that endothelin-1 is a vasoconstrictor in the human uterine artery and suggest that the effect is mediated by receptors on the smooth muscle cells. The mode of action seems to involve Ca++ influx by other than dihydropyridine-sensitive Ca++ channels. Endothelin-1 does not seem to stimulate release of other endothelium-derived vasoactive agents.
OBJECTIVE: The aim was to study the effects, mode of action, and binding sites of endothelin-1 in the human uterine artery. STUDY DESIGN: The contractile effect of endothelin-1 on the human uterine artery with and without endothelium and the effect of verapamil and nicardipine on the contraction was investigated in vitro. The Student t test was used. Iodine 125-endothelin-1 binding sites were localized with autoradiography. RESULTS:Endothelin-1 induced a contraction that was unaffected by removal of the endothelium. Verapamil antagonized the contraction, whereas nicardipine showed no effect. Iodine 125-endothelin-1 binding sites were demonstrated in the smooth muscle layer. CONCLUSIONS: These results show that endothelin-1 is a vasoconstrictor in the human uterine artery and suggest that the effect is mediated by receptors on the smooth muscle cells. The mode of action seems to involve Ca++ influx by other than dihydropyridine-sensitive Ca++ channels. Endothelin-1 does not seem to stimulate release of other endothelium-derived vasoactive agents.