Excitation-Contraction Coupling is Accomplished by Calcium Ions
Changes in Ca2+ permeability are shown in the bottom panel of Fig. 7. The initial depolarization of the membrane causes Ca2+ conductance to increase in a voltage-dependent manner. Unlike the sodium channels, the calcium channels are slow to close and there is a sustained increase in Ca2+ conductance, which maintains the plateau of the cardiac action potential. Another factor contributing to the plateau of the cardiac action potential is the change in K+ conductance (Fig. 7). At rest, the K+ conductance of cardiac cells is high, just as it is in nerve and skeletal muscle cells. The similarity, however, ends here. When nerve and muscle cells repolarize, a transient increase is observed in K+ conductance over the resting value, which quickly terminates the action potential and momentarily hyperpolarizes the cell. In contrast, in cardiac muscle K+ conductance decreases with depolarization (Fig. 7), and during repolarization K+ conductance simply returns to its phase 4 value. That is why cardiac muscle has no hyperpolarizing afterpotential. We should mention that there are many different types of potassium channels in the cardio-myocyte and their individual functions in controlling K+ conductance through the action potential are complex. A detailed description of these is beyond the scope of this chapter.
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