Héluy V, Fournier T, Cavaillé F, Germain G, Ferré F, Breuiller-Fouché M
Institut National de la Santé et de la Recherche Médicale, Université René-Descartes, Paris, France.
J Cardiovasc Pharmacol. 1995;26 Suppl 3:S138-41.
We investigated the contribution of endothelin (ET) ETA and ETB receptors to ET-induced contractions of human myometrium and their distribution in cultured myometrial cells. ET-1 was more potent than ET-3 in evoking concentration-dependent increases in smooth muscle tension. A selective ETB agonist, BQ 3020, was inactive in eliciting contractions. In myometrial cell membranes, no specific [125I]ET-3 binding was observed. Inhibition of [125I]ET-1 binding by unlabeled compounds showed the following order of potency: ET-1 = FR 139317 > ET-3 >> S6c. Furthermore, ET-1 increased inositol phosphate (IP) production in a dose-dependent manner. ET-1-induced IP accumulation was totally abolished by FR 139317 (an ETA-selective antagonist) but was not altered by IRL 1038 (an ETB-selective antagonist). These results indicate that only ETA receptors, which mediate ET-1-induced uterine contraction, are present in cultured myometrial cells.
我们研究了内皮素（ET）的ETA和ETB受体对ET诱导的人子宫肌层收缩的作用及其在培养的子宫肌层细胞中的分布。ET-1在引起平滑肌张力浓度依赖性增加方面比ET-3更有效。一种选择性ETB激动剂BQ 3020在引发收缩方面无活性。在子宫肌层细胞膜中，未观察到特异性的[125I]ET-3结合。未标记化合物对[125I]ET-1结合的抑制作用显示出以下效力顺序：ET-1 = FR 139317 > ET-3 >> S6c。此外，ET-1以剂量依赖性方式增加肌醇磷酸（IP）的产生。FR 139317（一种ETA选择性拮抗剂）完全消除了ET-1诱导的IP积累，但IRL 1038（一种ETB选择性拮抗剂）未改变其积累。这些结果表明，在培养的子宫肌层细胞中仅存在介导ET-1诱导子宫收缩的ETA受体。
