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维拉帕米和硝苯地平对人子宫动脉的“体外”作用。

Effects of verapamil and nifedipine on human uterine artery "in vitro".

作者信息

García de Boto M J, Hidalgo A, Andrés-Trelles F

机构信息

Farmacología. Dpto. de Medicina, Facultad de Medicina, Oviedo, Spain.

出版信息

Res Commun Chem Pathol Pharmacol. 1988 Nov;62(2):361-4.

PMID:2855183
Abstract

We have studied, in isolated human uterine arteries, the effects of verapamil and nifedipine on the contractions induced by noradrenaline (NA) and KCl in standard Krebs and those produced by CaCl2 and NA added to a free-calcium medium (128.5 mM K+). Both calcium antagonists reduce in a dose-dependent way the contractions induced by NA, KCl and CaCl2. Smaller doses of nifedipine were needed to produce the same inhibitory effects. The maximal doses of calcium antagonists utilized had no effect on the contractions induced by NA when the calcium was removed from the medium. NA, in equal doses, had similar contractile effect whether after incubation with the maximal doses of verapamil and nifedipine or in a calcium-free medium. The inhibitory effects produced by verapamil and nifedipine are only adequately explained by a blockage of the entry of calcium. Other intracellular changes do not seem to play a role in this case.

摘要

我们在离体的人子宫动脉中研究了维拉帕米和硝苯地平对去甲肾上腺素(NA)和氯化钾在标准 Krebs 液中所诱导的收缩,以及对添加到无钙培养基(128.5 mM K⁺)中的氯化钙和 NA 所产生的收缩的影响。两种钙拮抗剂均以剂量依赖性方式降低由 NA、氯化钾和氯化钙诱导的收缩。产生相同抑制作用所需的硝苯地平剂量较小。当从培养基中去除钙时,所使用的钙拮抗剂最大剂量对 NA 诱导的收缩没有影响。等量的 NA,无论与维拉帕米和硝苯地平的最大剂量孵育后还是在无钙培养基中,都具有相似的收缩作用。维拉帕米和硝苯地平产生的抑制作用仅通过阻断钙的内流才能得到充分解释。在这种情况下,其他细胞内变化似乎不起作用。

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