Indomethacin Depresses Prostaglandin F2α-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 F_2α (PGF_2α). Contraction to PGF_2α (0.1–30 μM) 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 μM) suppressed the maximum response to PGF_2α 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 μM) did not affect the response to PGF_2α. We conclude that the PGF_2α-induced contraction in guinea-pig uterine artery is mediated, at least in part, through constrictor non-thromboxane prostanoid(s) of vascular muscle origin.