Indomethacin reduces contraction of isolated non-pregnant human uterine artery induced by prostaglandin F2α

The purpose of this study was to explore whether cyclooxygenase products derived from endothelium or vascular smooth muscle participate in the response of human uterine artery to prostaglandin F2 alpha. Experiments were performed using human uterine arterial rings. Prostaglandin F2 alpha (0.4 nM-1 m...

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Bibliographic Details
Published in:Human reproduction (Oxford) 1996-09, Vol.11 (9), p.1998-2002
Main Authors: GRBOVIC, L, JOVANOVIC, A, TULIC, I
Format: Article
Language:English
Subjects:
Adult
Arteries - drug effects
Biological and medical sciences
Cyclooxygenase Inhibitors - pharmacology
Dinoprost - antagonists & inhibitors
Dinoprost - pharmacology
Dose-Response Relationship, Drug
Female
Fundamental and applied biological sciences. Psychology
Hormone metabolism and regulation
Humans
In Vitro Techniques
Indomethacin - pharmacology
Mammalian female genital system
Middle Aged
Osmolar Concentration
Uterus - blood supply
Vasoconstriction - drug effects
Vertebrates: reproduction
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Summary:The purpose of this study was to explore whether cyclooxygenase products derived from endothelium or vascular smooth muscle participate in the response of human uterine artery to prostaglandin F2 alpha. Experiments were performed using human uterine arterial rings. Prostaglandin F2 alpha (0.4 nM-1 microM) induced contraction of human uterine arteries with both intact and denuded endothelium with similar potency and efficacy (pD2 values: 7.93 +/- 0.01 and 8.07 +/- 0.03 for vessels with and without endothelium respectively; maximal response values: 89.1 +/- 4.7% and 92.3 +/- 3.8% for vessels with and without endothelium respectively). Indomethacin (10 microM) significantly suppressed the maximum effects of prostaglandin F2 alpha and induced a shift towards the right of the prostaglandin F2 alpha concentration-response curves, regardless of the endothelial condition. On the other hand, in both types of preparations, OKY-046 (10 microM), an inhibitor of thromboxane synthesis, did not affect prostaglandin F2 alpha-induced contraction of human uterine arteries. It is concluded that in human uterine artery prostaglandin F2 alpha-induced contraction is mediated, at least in part, through constrictor prostanoid(s) of vascular smooth muscle origin that is not thromboxane A2.
ISSN:0268-1161
1460-2350