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心肌老化有关心肌收缩和松弛等的亚细胞水平机理,现已完全清楚。在动作电位0相,钠经快通道流入细胞;在动作电位2相,钙经慢通道流入细胞,使其浓度梯度减小。细胞溶质内钙增加,促使细胞内贮存的钙从肌浆网释出。这种源自肌浆网的“钙触发性钙释放”(Calcium-triggered calcium release),使肌丝的调节蛋白(Troponin-tropomyosin)得以有更多的钙可供利用。结合于肌钙蛋白(Troponin)的钙,可使收缩蛋白肌纤蛋白和肌球蛋白(Actin和Myosin)的活性结合部位脱离空间抑制作用。收缩蛋白在肌球蛋白ATP酶(Myosin ATPase)的作用下,形成能量依赖
Myocardial Aging The mechanism of subcellular levels of myocardial contraction and relaxation is now fully understood. In action potential phase 0, sodium flows into the cells via fast channels; in the action potential phase 2, calcium flows into the cells through slow channels to decrease the concentration gradient. Increased intracellular calcium solutes, prompting the release of intracellular calcium from the sarcoplasmic reticulum. This calcium-triggered calcium release from the sarcoplasmic reticulum enables more calcium to be available to the troponin-tropomyosin. Binding to calcium of Troponin results in the steric hindrance of the active binding site of contracting proteins myosin and myosin (Actin and Myosin). Contraction protein in the myosin ATPase (Myosin ATPase) under the influence of the formation of energy-dependent