Electrophysiological feedback processes in skeletal and cardiac muscle excitation-contraction coupling
Christopher Huang, University of Cambridge
Abstract.
Skeletal and cardiac muscle excitation-contraction coupling begins with action potential generation and propagation driven by surface membrane sodium channels. This feeds forward into a dihydropyridine receptor triggered Ca2+ release through sarcoplasmic reticular membrane ryanodine receptors. Experimental studies on pro-arrhythmic genetic cardiac models implicate feedback actions of the resulting cytosolic Ca2+ increase on Na+ channel function. We review experimental criteria that these operate in native skeletal and cardiac muscle then demonstrate these predicted features, possibly underlying arrhythmia, in two murine catecholaminergic polymorphic ventricular tachycardic RyR2-P2328S and metabolically-deficient Pgc1β−/− cardiac models.
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