Endothelin-dependent vasoconstriction in XXXX uterine artery: application to @entity1468 .

@entity1 @entity63 @entity19346 @entity2232 @entity6555 @entity2514 @entity1627 @entity11345 @entity12833 @entity1468 @entity11344 @entity2231
BACKGROUND: Reduced uteroplacental perfusion, the initiating event in @entity1468 , is associated with enhanced @entity2232 ( @entity2232 ) production which feeds the vasoconstriction of uterine artery. Whether the treatments of @entity1468 were effective on @entity2232 induced contraction and could reverse placental @entity63 is the question addressed in this study. We investigated the effect of antihypertensive drugs used in @entity1468 and of ET receptor antagonists on the contractile response to @entity2232 on @entity1 uterine arteries. METHODOLOGY/PRINCIPAL FINDINGS: Experiments were performed, ex vivo, on @entity1 uterine artery samples obtained after hysterectomy. We studied variations in isometric tension of arterial rings in response to the vasoconstrictor @entity2232 and evaluated the effects of various vasodilators and ET-receptor antagonists on this response. Among antihypertensive drugs, only @entity19346 were effective in blocking and reversing the @entity2232 contractile response. Their efficiency, independent of the concentration of @entity2232 , was only partial. @entity2514 , @entity12833 and @entity6555 had no effect on @entity2232 induced contraction which is mediated by both @entity2231 and @entity1627 receptors in uterine artery. ET receptors antagonists, @entity11344 and @entity11345 , slightly reduced the amplitude of the response to @entity2232 . Combination of both antagonists was more efficient, but it was not possible to reverse the maximal @entity2232 -induced contraction with antagonists used alone or in combination. CONCLUSION: Pharmacological drugs currently used in the context of @entity1468 , do not reverse @entity2232 induced contraction. Only @entity19346 , which partially relax uterine artery previously contracted with @entity2232 , might offer interesting perspectives to improve placental perfusion.
