Roles and Regulation of Voltage-gated Calcium Channels in Arrhythmias

Figures

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  Figure 1:. Schematic of cardiac α1C, β, and α2 subunit topology. The β subunit binds to the α-interaction domain in the I–II loop of the α1C subunit. CaM binds to the C-terminus of α1C.

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  Figure 2:. Excitation–contraction coupling in cardiomyocytes. A and B: Ca2+ entry via CaV1.2 causes Ca2+-induced Ca2+ release via the ryanodine receptor (RyR2). C: Ca2+ binds to troponin C, inducing cross-bridging between actin and myosin. D: Ca2+ is pumped back into the sarcoplasmic reticulum via SERCA2a. The same amount of Ca2+ that enters the cell via CaV1.2 is pumped out of the cells via the Na+–Ca2+-exchanger and Ca2+ pumps (not shown). E: Ca2+ binds to CSQ in the sarcoplasmic reticulum.

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  Figure 3:. Diagram of cardiac action potential showing phases 0, 1, 2, 3, and 4. During phase 0, Na+ influx initiates the cardiac action potential. During phase 2, Ca2+ entry via the L-type Ca2+ channel initiates excitation–contraction coupling.