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[收缩性心脏。细胞和亚细胞层面]

[The contractile heart. Cellular and subcellular aspects].

作者信息

Larsen T H

机构信息

Institutt for anatomi og cellebiologi, Universitetet i Bergen.

出版信息

Tidsskr Nor Laegeforen. 1994 Dec 10;114(30):3636-40.

PMID:7825147
Abstract

The excitation-contraction coupling can be defined as the mechanisms involved when the action potential initiates a contraction response of the cardiac muscle cell. The action potential is conducted from cell to cell, resulting in a synchronized contraction of the myocardium. Both the propagation of the action potential and the myofibrillar contraction are dependent on changes in free Ca++ concentrations. Recently, the mediators and the molecular and structural components involved in the subcellular transforming of the action potential into a contraction have been characterized. The opening of voltage-dependent L-type Ca(++)-channels in the cell membrane stimulates a release of Ca++ from the sarcoplasmic reticulum. This Ca(++)-mediated Ca(++)-release appears to be a graded mechanism and is associated with the presence of structural couplings (Ca++ synapses) in the cardiac muscle cell.

摘要

兴奋-收缩偶联可定义为动作电位引发心肌细胞收缩反应时所涉及的机制。动作电位在细胞间传导,导致心肌同步收缩。动作电位的传播和肌原纤维收缩均依赖于游离Ca++浓度的变化。最近,参与将动作电位亚细胞转化为收缩的介质以及分子和结构成分已得到表征。细胞膜中电压依赖性L型Ca(++)通道的开放刺激肌浆网释放Ca++。这种Ca(++)介导的Ca(++)释放似乎是一种分级机制,并且与心肌细胞中结构偶联(Ca++突触)的存在有关。

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