Excitation-contraction coupling gain in ventricular myocytes: insights from a parsimonious model.
Excitation-contraction coupling gain in ventricular myocytes: insights from a parsimonious model.
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心室肌细胞的兴奋-收缩耦合增益：来自简约模型的见解。
DOI：
10.1113/jphysiol.2008.163915
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Ramay,HenaR
中科院分区：
文献类型：
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作者：
Sobie,EricA;Ramay,HenaR
我们提出了心室肌细胞电压钳条件下钙火花触发的最小数学模型。该模型预测的变化，兴奋收缩耦合的“增益”，从不同的实验干预的结果。我们比较模型的结果，几组数据，并在这样做，把明显的生理相关的模型参数的限制。具体来说，分析表明，许多L-型Ca 2+通道开放可能会触发每个Ca 2+火花，但单个开放触发火花的可能性很低。这一过程有助于调和矛盾的结果，在最近的研究中，此外，这个新的模型应该是一个有用的工具，了解发生在生理和疾病的增益变化。
We present a minimal mathematical model of Ca2+spark triggering under voltage‐clamp conditions in ventricular myocytes. The model predicts changes in excitation–contraction coupling ‘gain’ that result from diverse experimental interventions. We compare model results to several sets of data, and, in so doing, place apparent constraints on physiologically relevant model parameters. Specifically, the analysis suggests that many L‐type Ca2+channel openings can potentially trigger each Ca2+spark, but the probability that an individual opening will trigger a spark is low. This procedure helps to reconcile contradictory results obtained in recent studies; moreover, this new model should be a useful tool for understanding changes in gain that occur physiologically and in disease.