Uterus and endometrium: Indomethacin reduces contraction of isolated non-pregnant human uterine artery induced by prostaglandin F2α

• Published in: Human reproduction (Oxford) 1996-09, Vol.11 (9), p.1998-2002
• Main Authors: Grbović, Leposava, Jovanović, Aleksandar, Tulić, Ivan
• Format: Article
• Language: English
• Subjects: endothelium; F2α artery; indomethacin; OKY-046; prostaglandin
• ISSN: 0268-1161; 1460-2350
• DOI: 10.1093/oxfordjournals.humrep.a019532

The purpose of this study was to explore whether cyclo oxygenase products derived from endothelium or vascular smooth muscle participate In the response of human uterine artery to prostaglandin F2α Experiments were performed using human uterine arterial rings. Prostaglandin F2α (0.4 nM-1 μM) induced contraction of human uterine arteries with both Intact and denuded endothellum with similar potency and efficacy (pD2 values: 7.93±0.01 and 8.07±0.03 for vessels with and without endotheliuin respectively; maximal response values: 89.1±4.7% and 92.3±3.8% for vessels with and without endotheliuin respectively). Indomethacin (10 μM) significantly sup pressed the maximum effects of prostaglandin F2α and induced a shift towards the right of the prostaglandin F2α concentration-response curves, regardless of the endo thelial condition. On the other hand, in both types of preparations, OKY-046 (10 μM), an inhibitor of throm boxane synthesis, did not affect prostaglandin F2α-induced contraction of human uterine arteries. It is concluded that in human uterine artery prostaglandin F2α-induced contraction is mediated, at least in part, through constrictor prostanoid(s) of vascular smooth muscle origin that is not thromboxane A2.