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硝苯地平和BAY K抑制收缩,与其对钙通道的作用无关。

Nifedipine and BAY K inhibit contraction independently from their action on calcium channels.

作者信息

Jacquemond V, Rougier O

机构信息

Laboratoire de Physiologie des Eléments Excitables (CNRS UA 244), Université Claude Bernard, Villeurbanne, France.

出版信息

Biochem Biophys Res Commun. 1988 May 16;152(3):1002-7. doi: 10.1016/s0006-291x(88)80383-8.

Abstract

Voltage-clamp experiments were performed on twitch skeletal muscle fibres in a double sucrose-gap device in order to investigate the effect of 1,4-dihydropyridines (DHP) on excitation-contraction coupling during 50 ms step depolarizations. External solution used was free of permeant anions and contained only Ca++ as permeant cation. It is shown that in these conditions Nifedipine (a Ca++ channel antagonist) and BAY K 8644 (a Ca++ channel agonist) inhibit contraction in a way independent of their action on the gating of tubular calcium channels. These results indicate also that a close relation between DHP receptors and calcium channels must be taken with caution.

摘要

在双蔗糖间隙装置中对单收缩骨骼肌纤维进行电压钳实验,以研究1,4 - 二氢吡啶(DHP)在50毫秒阶跃去极化期间对兴奋 - 收缩偶联的影响。所用的外部溶液不含渗透性阴离子,仅含有Ca++作为渗透性阳离子。结果表明,在这些条件下,硝苯地平(一种Ca++通道拮抗剂)和BAY K 8644(一种Ca++通道激动剂)以与其对管状钙通道门控作用无关的方式抑制收缩。这些结果还表明,必须谨慎对待DHP受体与钙通道之间的密切关系。

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