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由于肌浆网Ca2+-ATP酶活性导致的青蛙骨骼肌纤维收缩电压激活的变化。

Changes in voltage activation of contraction in frog skeletal muscle fibres as a result of sarcoplasmic reticulum Ca2+-ATPase activity.

作者信息

Même W, Léoty C

机构信息

Laboratoire de Physiologie Générale, CNRS EP1593, Faculté des Sciences et des Techniques, 2 Rue de la Houssinière, Nantes Cedex 3, France.

出版信息

Acta Physiol Scand. 1999 Jul;166(3):209-16. doi: 10.1046/j.1365-201x.1999.00551.x.

DOI:10.1046/j.1365-201x.1999.00551.x
PMID:10468657
Abstract

The effects of cyclopiazonic acid, a specific sarcoplasmic reticulum Ca2+-ATPase inhibitor, on isometric tension were studied in response to prolonged steady-state depolarization induced by a rapid change in extracellular potassium concentration (potassium contractures) in frog semitendinosus muscle fibres. Cyclopiazonic acid (1-10 microM) enhanced the amplitude and time-course of relaxation of 146 mM potassium contracture. In the presence of cyclopiazonic acid 0.5 microM, the relationship between the amplitude of potassium contractures and the membrane potential shifted to more negative potentials, whereas the steady-state inactivation curve was unchanged. These observations suggest that cyclopiazonic acid has no effect on voltage sensors. The difference between potassium contractures in the absence and presence of cyclopiazonic acid in skeletal muscle fibres implies that the amplitude and slow relaxation of tension during prolonged steady-state depolarization may be expected to depend not only on inactivation of the process regulating calcium release from the sarcoplasmic reticulum but also on the ability of the sarcoplasmic reticulum to pump calcium.

摘要

研究了特异的肌浆网Ca2 + -ATP酶抑制剂环匹阿尼酸对青蛙半腱肌纤维因细胞外钾浓度快速变化诱导的长时间稳态去极化(钾挛缩)所产生的等长张力的影响。环匹阿尼酸(1 - 10微摩尔)增强了146毫摩尔钾挛缩的舒张幅度和时程。在存在0.5微摩尔环匹阿尼酸的情况下,钾挛缩幅度与膜电位之间的关系向更负的电位偏移,而稳态失活曲线未改变。这些观察结果表明环匹阿尼酸对电压传感器无影响。骨骼肌纤维在不存在和存在环匹阿尼酸时钾挛缩的差异意味着,在长时间稳态去极化期间,张力的幅度和缓慢舒张可能不仅取决于调节肌浆网钙释放过程的失活,还取决于肌浆网泵钙的能力。

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