| Abstract | Recent investigations into the structure and function of cardiac caveolae, small invaginations of a cardiomyocyte’s plasma membrane, reveal that treatment of a myocyte with a beta-agonist opens caveolar necks and presents the sarcolemma with additional sodium ion channels. As such, caveolae constitute a substantial and previously unrecognized source of sodium current that can significantly influence cardiac action potential morphology and the conduction velocity of the excitatory wave front. In this work, we formulate a model of cardiac action potential that incorporates stochastic caveolar dynamics and simulate the effects of caveolar sodium current on the action potential. In particular, we use this model to suggest that in pathological cases, caveolae may play a role the development of the late persistent sodium current known to cause the cardiac arrhythmia called long Q-T syndrome. |
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