Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Department of Physiology, University of Auckland, Auckland, New Zealand.
Acta Physiol (Oxf). 2019 May;226(1):e13250. doi: 10.1111/apha.13250. Epub 2019 Jan 25.
When exposed to an abrupt stretch, cardiac muscle exhibits biphasic active force enhancement. The initial, instantaneous, force enhancement is well explained by the Frank-Starling mechanism. However, the cellular mechanisms associated with the second, slower phase remain contentious. This review explores hypotheses regarding this "slow force response" with the intention of clarifying some apparent contradictions in the literature. The review is partitioned into three sections. The first section considers pathways that modify the intracellular calcium handling to address the role of the sarcoplasmic reticulum in the mechanism underlying the slow force response. The second section focuses on extracellular calcium fluxes and explores the identity and contribution of the stretch-activated, non-specific, cation channels as well as signalling cascades associated with G-protein coupled receptors. The final section introduces promising candidates for the mechanosensor(s) responsible for detecting the stretch perturbation.
当心肌暴露于突然的拉伸时，会表现出双相的主动力增强。最初的瞬时力增强可以很好地用弗兰克-斯塔尔林机制来解释。然而，与第二相（较慢）相关的细胞机制仍存在争议。本综述探讨了关于这种“缓慢力反应”的假说，旨在澄清文献中的一些明显矛盾。综述分为三个部分。第一部分考虑了修饰细胞内钙处理的途径，以解决肌浆网在缓慢力反应机制中的作用。第二部分侧重于细胞外钙流，并探讨了伸展激活的非特异性阳离子通道的特性和贡献，以及与 G 蛋白偶联受体相关的信号级联。最后一部分介绍了负责检测拉伸扰动的机械感受器（s）的有希望的候选者。
