Stretch modulation of cardiac contractility: importance of myocyte calcium during the slow force response.
Stretch modulation of cardiac contractility: importance of myocyte calcium during the slow force response.
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DOI：
10.1007/s12551-020-00615-6
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发表时间：
2020-02-01
影响因子：
--
通讯作者：
Ward, Marie-Louise
中科院分区：
文献类型：
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作者：
Kaur, Sarbjot;Shen, Xin;Ward, Marie-Louise
自从100多年前肌肉生理学家的工作以来，心脏对心肌牵张的机械反应已经被理解，即在收缩期间心室腔充盈的增加增加了随后的收缩力。牵张引起的收缩增加是双相的。有一个突然增加的力量，与拉伸（快速反应），然后由一个较慢的反应，发展了几分钟（缓慢的力反应，或SFR）。SFR与Ca2+瞬变幅度的逐渐增加相关，这是启动肌细胞跨桥循环和力发展的事件。然而，拉伸依赖性增加的Ca2+瞬变的机制仍有争议。本文综述了近年来有关SFR的文献，并总结了不同的牵张激活Ca2+进入途径。SFR可能是由响应于不同细胞拉伸传感器的激活而启动的几种不同细胞机制的组合引起的。
The mechanical response of the heart to myocardial stretch has been understood since the work of muscle physiologists more than 100years ago, whereby an increase in ventricular chamber filling during diastole increases the subsequent force of contraction. The stretch-induced increase in contraction is biphasic. There is an abrupt increase in the force that coincides with the stretch (the rapid response), which is then followed by a slower response that develops over several minutes (the slow force response, or SFR). The SFR is associated with a progressive increase in the magnitude of the Ca2+ transient, the event that initiates myocyte cross-bridge cycling and force development. However, the mechanisms underlying the stretch-dependent increase in the Ca2+ transient are still debated. This review outlines recent literature on the SFR and summarizes the different stretch-activated Ca2+ entry pathways. The SFR might result from a combination of several different cellular mechanisms initiated in response to activation of different cellular stretch sensors.