INDOMETHACIN DEPRESSES PROSTAGLANDIN F-2-ALPHA-INDUCED CONTRACTION INGUINEA-PIG UTERINE ARTERY WITH BOTH INTACT AND DENUDED ENDOTH

The purpose of this study was to explore whether cyclooxygenase produc ts derived from endothelium or vascular muscle participate in the resp onse of guinea-pig uterine arterial rings to prostaglandin F-2 alpha ( PGF(2 alpha)). Contraction to PGF(2 alpha) (0.1-30 mu M) occurred with and without endothelium at similar potency and efficacy (pEC(50) (-lo g EC50) values respectively 5.87 +/- 0.06 and 5.97 +/- 0.07; maximal r esponse respectively 78.2 +/- 1.3% and 76.9 +/- 1.5% of contraction in duced by 126 mM KCl). Indomethacin (3-30 mu M) suppressed the maximum response to PGF(2 alpha) and induced a rightward shift of concentratio n-response curves, regardless of the presence of endothelium. pIC(50) values for indomethacin were 4.67 and 4.74 for vessels with and withou t endothelium, respectively. In contrast, the thromboxane synthesis in hibitor OKY-046 (10 and 100 mu M) did not affect the response to PGF(2 alpha). We conclude that the PGF(2 alpha)-induced contraction in guin ea-pig uterine artery is mediated, at least in part, through constrict or non-thromboxane prostanoid(s) of vascular muscle origin.