Indomethacin depresses prostaglandin F2 alpha-induced contraction in guinea-pig uterine artery with both intact and denuded endoth.

The purpose of this study was to explore whether cyclooxygenase products derived from endothelium or vascular muscle participate in the response of guinea-pig uterine arterial rings to prostaglandin F2 alpha (PGF2 alpha). Contraction to PGF2 alpha (0.1-30 microM) occurred with and without endothelium at similar potency and efficacy (pEC50 (-log EC50) values respectively 5.87 +/- 0.06 and 5.97 +/- 0.07; maximal response respectively 78.1 +/- 1.3% and 76.9 +/- 1.5% of contraction induced by 126 mM KCl). Indomethacin (3-30 microM) suppressed the maximum response to PGF2 alpha and induced a rightward shift of concentration-response curves, regardless of the presence of endothelium. pIC50 values for indomethacin were 4.67 and 4.74 for vessels with and without endothelium, respectively. In contrast, the thromboxane synthesis inhibitor OKY-046 (10 and 100 microM) did not affect the response to PGF2 alpha. We conclude that the PGF2 alpha-induced contraction in guinea-pig uterine artery is mediated, at least in part, through constrictor non-thromboxane prostanoid(s) of vascular muscle origin.