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氯化亚锡与钙通道阻滞剂在青蛙神经肌肉传递中的相互作用。

Interaction between stannous chloride and calcium channel blockers in frog neuromuscular transmission.

作者信息

Hattori T, Maehashi H

机构信息

Department of Dental Pharmacology, Matsumoto Dental College, Shiojiri, Japan.

出版信息

Res Commun Chem Pathol Pharmacol. 1992 Feb;75(2):243-6.

PMID:1315065
Abstract

We have investigated the interactions between stannous chloride (SnCl2) and calcium (Ca) channel blockers on endplate potentials (e.p.p.) and on miniature endplate potentials (m.e.p.p.) to determine which type of channel (among L-, N-, and T-type) participates in the SnCl2-induced increase in Ca entry into motor nerve terminals. The e.p.p. amplitude augmented by 30 microM SnCl2 was decreased by cumulative addition of 10 microM CdCl2 or 0.5 microM omega-conotoxin but not by 10 microM NiCl2 or 5 microM nicardipine. The SnCl2 (30 microM)-induced rise in m.e.p.p. frequency in high-potassium medium was reduced by 0.5 microM omega-conotoxin but not by 5 microM nicardipine. These results suggest that activation of the N-type Ca channel is involved in the SnCl2-induced increase in Ca entry into the nerve terminals.

摘要

我们研究了氯化亚锡(SnCl2)与钙(Ca)通道阻滞剂对终板电位(e.p.p.)和微小终板电位(m.e.p.p.)的相互作用,以确定哪种类型的通道(L型、N型和T型)参与了SnCl2诱导的运动神经末梢钙内流增加。30微摩尔SnCl2增强的e.p.p.幅度,在累积添加10微摩尔CdCl2或0.5微摩尔ω-芋螺毒素后降低,但在添加10微摩尔NiCl2或5微摩尔尼卡地平时未降低。在高钾培养基中,30微摩尔SnCl2诱导的m.e.p.p.频率升高,在添加0.5微摩尔ω-芋螺毒素后降低,但在添加5微摩尔尼卡地平时未降低。这些结果表明,N型钙通道的激活参与了SnCl2诱导的神经末梢钙内流增加。

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