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Mechanism of Ca/sup ++/ release from the myocyte sarcoplasmic reticulum: a model study

机译:Ca / sup ++ /从肌细胞肌浆网中释放的机制:模型研究

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The mechanism of Ca/sup ++/ release from the cardiac sarcoplasmic reticulum (SR) is still uncertain. It is assumed here that the release of Ca/sup ++/ from the SR is mainly regulated by the kinetics of Ca/sup ++/ channels within the SR membrane. These kinetics are controlled, under physiological conditions, by changes in the concentration of free Ca/sup ++/ near the openings of Ca/sup ++/ channels, and are affected by Ca/sup ++/ competitors, e.g. ryanodine. The study describes this control mechanism by a combination of positive and negative control loops, associated with two types of Ca/sup ++/ binding sites located on the SR membrane: (1) activating sites with low affinity to Ca/sup ++/ and high binding rare, and (2) inactivating sites with high affinity but low binding rate. This model successfully describes the process of Ca/sup ++/ release from the SR. The ryanodine intervention supports the hypothesis of the control mechanism described by the model.
机译:Ca / sup ++ /从心脏肌浆网(SR)释放的机制仍不确定。这里假设Ca / sup ++ /从SR的释放主要受SR膜内Ca / sup ++ /通道的动力学调节。在生理条件下,这些动力学通过Ca / sup ++ /通道开口附近的游离Ca / sup ++ /浓度的变化来控制,并受Ca / sup ++ /竞争剂的影响。 ryanodine。该研究通过正向控制回路和负向控制回路的组合来描述这种控制机制,该控制回路与位于SR膜上的两种类型的Ca / sup ++ /结合位点相关:(1)激活对Ca / sup ++ /的亲和力低的位点(2)具有高亲和力但结合率低的失活位点。该模型成功描述了从SR释放Ca / sup ++ /的过程。 ryanodine干预支持该模型描述的控制机制的假设。

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