Davis Jonathan P, Tikunova Svetlana B
Department of Physiology and Cell Biology, The Ohio State University, 400 Hamilton Hall, Columbus, OH 43210, USA.
Cardiovasc Res. 2008 Mar 1;77(4):619-26. doi: 10.1093/cvr/cvm098. Epub 2007 Dec 12.
Controversy abounds in the cardiac muscle literature over the rate-limiting steps of cardiac muscle contraction and relaxation. However, the idea of a single biochemical mechanism being the all-inclusive rate-limiting step for cardiac muscle contraction and relaxation may be oversimplified. There is ample evidence that Ca(2+) concentration and dynamics, intrinsic cross-bridge properties, and even troponin C (TnC) Ca(2+) binding and dissociation can all modulate the mechanical events of cardiac muscle contraction and relaxation. However, TnC has generally been thought to play no role in influencing cardiac muscle dynamics due to the idea that Ca(2+) exchange with TnC is very rapid. This definitely is the case for isolated TnC, but not for the more sophisticated biochemical systems of reconstituted thin filaments and myofibrils. This review will discuss the biochemical influences on Ca(2+) exchange with TnC and their physiological implications.
在心肌收缩和舒张的限速步骤方面，心肌文献中存在诸多争议。然而，认为单一生化机制是心肌收缩和舒张的唯一限速步骤的观点可能过于简单化。有充分证据表明，钙离子（Ca(2+)）浓度和动力学、内在横桥特性，甚至肌钙蛋白C（TnC）与Ca(2+)的结合和解离都能调节心肌收缩和舒张的机械事件。然而，由于与TnC的Ca(2+)交换非常迅速这一观点，TnC通常被认为在影响心肌动力学方面不起作用。对于分离的TnC确实如此，但对于重组细肌丝和肌原纤维等更复杂的生化系统则并非如此。本综述将讨论对与TnC进行Ca(2+)交换的生化影响及其生理意义。
