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本文引用的文献

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Altered interactions among thin filament proteins modulate cardiac function.细肌丝蛋白之间相互作用的改变会调节心脏功能。
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Intrinsic myofilament alterations underlying the decreased contractility of stunned myocardium. A consequence of Ca2+-dependent proteolysis?顿抑心肌收缩力降低背后的肌丝内在改变。钙依赖性蛋白水解的结果?
Circ Res. 1996 Mar;78(3):455-65. doi: 10.1161/01.res.78.3.455.
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Ca2+ and segment length dependence of isometric force kinetics in intact ferret cardiac muscle.雪貂完整心肌中静息肌力动力学的钙离子(Ca2+)和节段长度依赖性
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4
Role of troponin C in determining the Ca(2+)-sensitivity and cooperativity of the tension development in rabbit skeletal and cardiac muscles.肌钙蛋白C在决定兔骨骼肌和心肌中张力发展的钙(2+)敏感性和协同性方面的作用。
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Length, force, and Ca(2+)-troponin C affinity in cardiac and slow skeletal muscle.心肌和慢肌中肌节长度、力及钙离子-肌钙蛋白C亲和力
Am J Physiol. 1994 Apr;266(4 Pt 1):C1077-82. doi: 10.1152/ajpcell.1994.266.4.C1077.
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Coupling calcium binding to troponin C and cross-bridge cycling in skinned cardiac cells.在分离的心肌细胞中将钙结合与肌钙蛋白C及横桥循环相偶联。
Am J Physiol. 1994 Mar;266(3 Pt 2):H1260-71. doi: 10.1152/ajpheart.1994.266.3.H1260.
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Rate of tension development in cardiac muscle varies with level of activator calcium.心肌中张力发展的速率随激活钙水平而变化。
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Kinetics of tension development in skinned cardiac myocytes measured by photorelease of Ca2+.通过Ca2+光释放测量的去表皮心肌细胞中张力发展的动力学。
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The regulatory switch of the muscle thin filament: Ca2+ or myosin heads?肌肉细肌丝的调节开关:钙离子还是肌球蛋白头部?
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Dynamics of the muscle thin filament regulatory switch: the size of the cooperative unit.肌肉细肌丝调节开关的动力学:协同单位的大小。
Biophys J. 1994 Jul;67(1):273-82. doi: 10.1016/S0006-3495(94)80478-3.

肌肉力量重建的速率常数反映了协同激活以及横桥动力学。

Rate constant of muscle force redevelopment reflects cooperative activation as well as cross-bridge kinetics.

作者信息

Campbell K

机构信息

Department of Veterinary and Comparative Anatomy, Physiology, and Pharmacology, Washington State University, Pullman 99164, USA.

出版信息

Biophys J. 1997 Jan;72(1):254-62. doi: 10.1016/S0006-3495(97)78664-8.

DOI:10.1016/S0006-3495(97)78664-8
PMID:8994610
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1184314/
Abstract

The rate of muscle force redevelopment after release-restretch protocols has previously been interpreted using a simple two-state cross-bridge cycling model with rate constants for transitions between non-force-bearing and force-bearing states, f, and between force-bearing and non-force-bearing states, g. Changes in the rate constant of force redevelopment, as with varying levels of Ca2+ activation, have traditionally been attributed to Ca(2+)-dependent f. The current work adds to this original model a state of unactivated, noncycling cross-bridges. The resulting differential equation for activated, force-bearing cross-bridges, Ncf, was Ncf = -[g+f(K/(K + 1))] Ncf+f(K/(K + 1))NT, where K is an equilibrium constant defining the distribution between cycling and noncycling cross-bridges and NT is the total number of cross-bridges. Cooperativity by which force-bearing cross-bridges participate in their own activation was introduced by making K depend on Ncf. Model results demonstrated that such cooperativity, which tends to enhance force generation at low levels of Ca2+ activation, has a counter-intuitive effect of slowing force redevelopment. These dynamic effects of cooperativity are most pronounced at low Ca2+ activation. As Ca2+ activation increases, the cooperative effects become less important to the dynamics of force redevelopment and, at the highest levels of Ca2+ activation, the dynamics of force redevelopment reflect factors other than cooperative mechanisms. These results expand on earlier interpretations of Ca2+ dependence of force redevelopment; rather than Ca(2+)-dependent f, Ca(2+)-dependent force redevelopment arises from changing expressions of cooperativity between force-bearing cross-bridges and activation.

摘要

先前,释放 - 拉伸方案后肌肉力量重新发展的速率是使用一个简单的双态横桥循环模型来解释的,该模型具有非承载和承载状态之间转换的速率常数f,以及承载和非承载状态之间转换的速率常数g。与不同水平的Ca2 + 激活一样,力量重新发展速率常数的变化传统上归因于Ca(2 +)依赖性f。当前的工作在这个原始模型中增加了未激活的、非循环横桥的状态。由此产生的关于激活的、承载力量的横桥Ncf的微分方程为Ncf = -[g + f(K / (K + 1))] Ncf + f(K / (K + 1))NT,其中K是定义循环和非循环横桥之间分布的平衡常数,NT是横桥的总数。通过使K依赖于Ncf,引入了承载力量的横桥参与自身激活的协同性。模型结果表明,这种协同性在低水平的Ca2 + 激活时倾向于增强力量产生,但对力量重新发展具有减缓作用,这一作用与直觉相反。协同性的这些动态效应在低Ca2 + 激活时最为明显。随着Ca2 + 激活增加,协同效应对于力量重新发展的动力学变得不那么重要,并且在最高水平的Ca2 + 激活时,力量重新发展的动力学反映了协同机制以外的因素。这些结果扩展了早期对力量重新发展的Ca2 + 依赖性的解释;力量重新发展的Ca(2 +)依赖性不是源于Ca(2 +)依赖性f,而是源于承载力量的横桥与激活之间协同性表达的变化。