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.