Abstract
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 (pEC 50 (−log EC 50) 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. pIC 50 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.
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