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豚鼠心室肌动作电位期间去极化增强收缩的机制。

Mechanism of potentiation of contraction by depolarization during action potentials in guinea-pig ventricular muscle.

作者信息

Terrar D A, White E

机构信息

University Department of Pharmacology, Oxford.

出版信息

Q J Exp Physiol. 1989 May;74(3):355-8. doi: 10.1113/expphysiol.1989.sp003277.

DOI:10.1113/expphysiol.1989.sp003277
PMID:2748796
Abstract

Action potentials were recorded from guinea-pig ventricular cells and contraction recorded by an optical technique. When the plateau of a single action potential was depolarized (by 70-120 pA applied 100 ms after the upstroke for 100 ms), contraction associated with the following normal action potential was potentiated. This potentiation was not seen in cells exposed to 10 mM-caffeine. The observations are consistent with potentiation of subsequent contraction by increased loading of caffeine-sensitive calcium stores, as a consequence of reduced Ca2+ extrusion or possibly Ca2+ entry via Na+-Ca2+ exchange during a depolarized plateau.

摘要

从豚鼠心室细胞记录动作电位,并通过光学技术记录收缩情况。当单个动作电位的平台期去极化时(在动作电位上升支后100毫秒施加70 - 120 pA,持续100毫秒),与随后正常动作电位相关的收缩增强。在暴露于10 mM咖啡因的细胞中未观察到这种增强现象。这些观察结果与去极化平台期期间钙外流减少或可能通过钠 - 钙交换的钙内流导致咖啡因敏感性钙储存增加从而增强后续收缩相一致。

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