Indomethacin reduces contraction of isolated non-pregnant human uterine artery induced by prostaglandin F(2α)

Abstract

The purpose of this study was to explore whether cyclooxygenase products derived from endothelium or vascular smooth muscle participate in the response of human uterine artery to prostaglandin F(2α). Experiments were performed using human uterine arterial rings. Prostaglandin F(2α) (0.4 nM-1 μM) induced contraction of human uterine arteries with both intact and denuded endothelium with similar potency and efficacy (pD2 values: 7.93 ± 0.01 and 8.07 ± 0.03 for vessels with and without endothelium respectively; maximal response values: 89.1 ± 4.7% and 92.3 ± 3.8% for vessels with and without endothelium respectively). Indomethacin (10 μM) significantly suppressed the maximum effects of prostaglandin F(2α) and induced a shift towards the right of the prostaglandin F(2α) concentration-response curves, regardless of the endothelial condition. On the other hand, in both types of preparations, OKY-046 (10 μM), an inhibitor of thromboxane synthesis, did not affect prostaglandin F(2α)-induced contraction of human uterine arteries. It is concluded that in human uterine artery prostaglandin F(2α)-induced contraction is mediated, at least in part, through constrictor prostanoid(s) of vascular smooth muscle origin that is not thromboxane A2.