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硫柳汞以一种内皮依赖性方式使动脉平滑肌超极化。

Thimerosal hyperpolarizes arterial smooth muscles in an endothelium-dependent manner.

作者信息

Bény J L

机构信息

Départment de Biologie Animale, Université de Genève, Switzerland.

出版信息

Eur J Pharmacol. 1990 Aug 28;185(2-3):235-8. doi: 10.1016/0014-2999(90)90647-o.

Abstract

Thimerosal activates the production of endothelium-derived relaxing factor (EDRF). I examined whether thimerosal also causes the release of an endothelium-dependent hyperpolarizing factor (EDHF). Thimerosal caused an endothelium-dependent hyperpolarization of smooth muscle. This effect is unlikely to be caused by the property of thimerosal to inhibit the acyl-coenzyme A: lysolecithin acyltransferase (LAT) since neither arachidonic acid nor lysolecithin hyperpolarized the muscles. I conclude that thimerosal is not a pure activator of EDRF (nitric oxide) production, but that it also releases a distinct EDHF.

摘要

硫柳汞可激活内皮源性舒张因子(EDRF)的生成。我研究了硫柳汞是否还会引起内皮依赖性超极化因子(EDHF)的释放。硫柳汞可引起平滑肌的内皮依赖性超极化。这种效应不太可能是由硫柳汞抑制酰基辅酶A:溶血卵磷脂酰基转移酶(LAT)的特性引起的,因为花生四烯酸和溶血卵磷脂均未使肌肉超极化。我得出结论,硫柳汞不是EDRF(一氧化氮)生成的单纯激活剂,而是还会释放一种独特的EDHF。

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