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首页> 外文期刊>American Journal of Physiology >Ca transients from Ca channel activity in rat cardiac myocytes reveal dynamics of dyad cleft and troponin C Ca binding.
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Ca transients from Ca channel activity in rat cardiac myocytes reveal dynamics of dyad cleft and troponin C Ca binding.

机译：大鼠心肌细胞中Ca通道活性引起的Ca瞬变揭示了成对裂和肌钙蛋白C Ca结合的动力学。

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摘要

The properties of the dyad cleft can in principle significantly impact excitation-contraction coupling, but these properties are not easily amenable to experimental investigation. We simultaneously measured the time course of the rise in integrated Ca current (ICa) and the rise in concentration of fura 2 with Ca bound ([Ca-fura 2]) with high time resolution in rat myocytes for conditions under which Ca entry is only via L-type Ca channels and sarcoplasmic reticulum (SR) Ca release is blocked, and compared these measurements with predictions from a finite-element model of cellular Ca diffusion. We found that 1) the time course of the rise of [Ca-fura 2] follows the time course of integrated ICa plus a brief delay (1.36 +/- 0.43 ms, n = 6 cells); 2) from the model, high-affinity Ca binding sites in the dyad cleft at the level previously envisioned would result in a much greater delay (>/=3 ms) and are therefore unlikely to be present at that level; 3) including ATP in the model promoted Ca efflux from the dyad cleft by a factor of 1.57 when low-affinity cleft Ca binding sites were present; 4) the data could only be fit to the model if myofibrillar troponin C (TnC) Ca binding were low affinity (4.56 microM), like that of soluble troponin C, instead of the high-affinity value usually used (0.38 microM). In a "good model," the rate constants for Ca binding and dissociation were 0.375 times the values for soluble TnC; and 5) consequently, intracellular Ca buffering at the rise of the Ca transient is inferred to be low.
机译：二分体裂隙的特性原则上可以显着影响激励-收缩耦合，但是这些特性不容易进行实验研究。我们以高时间分辨率同时测量了仅进入钙的情况下大鼠心肌细胞中整合钙电流（ICa）上升和结合有钙的呋喃2（[Ca-fura 2]）浓度升高的时间过程。通过L型Ca通道和肌浆网（SR），Ca释放被阻止，并将这些测量结果与细胞Ca扩散的有限元模型的预测结果进行比较。我们发现1）[Ca-fura 2]上升的时间过程遵循积分ICa的时间过程加上短暂的延迟（1.36 +/- 0.43 ms，n = 6个单元）; 2）根据模型，在二分体裂隙中的高亲和力Ca结合位点处于先前设想的水平将导致更大的延迟（> / = 3 ms），因此不太可能出现在该水平上; 3）当存在低亲和力的裂隙钙结合位点时，在模型中包括ATP可以促进二分体裂隙的Ca外排1.57倍; 4）仅当肌原纤维网肌钙蛋白C（TnC）Ca结合为低亲和力（4.56 microM）（如可溶性肌钙蛋白C）而不是通常使用的高亲和力值（0.38 microM）时，数据才能适合模型。在一个“好的模型”中，Ca结合和解离的速率常数是可溶性TnC值的0.375倍。 5）因此，推断Ca瞬变上升时的细胞内Ca缓冲低。

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