Prolonged Opening Of Calcium Channel Causes The Plateau Phase Of The Action Potential

In a nerve cell or a muscle cell, a rapid increase in Na+ permeability (actually conductance, because we are talking about charge movement) is seen that depolarizes the cell, followed by an increase in K+ conductance that repolarizes it. The peculiar shape of the cardiac action potential suggests that the ionic mechanisms are different in heart cells, as indeed they are. Figure 6A shows an action potential from a normal contractile cell, whereas Fig. 6B shows the action potential after treating the cell with tetrodotoxin (TTX). TTX selectively blocks the voltage-gated fast sodium channels. TTX does not completely block the action potential, as it does in nerve or muscle; rather, it only attenuates the rate of phase 0 depolarization. Clearly, a sustained increased Na+ conductance is not what prolongs the duration of the cardiac action potential.

The long plateau phase is actually due to a prolonged increase in Ca2+ conductance through voltage-dependent calcium channels, often referred to as L-type calcium channels. These channels are similar to those seen in the presynaptic terminal (Chapter 6) or in smooth muscle (Chapter 8). An increase in Ca2+ permeability will depolarize the cell just as an increase in Na+ permeability does. The concentration of Ca2+ is much higher outside the cell than inside, with an equilibrium potential of about +120 mV. Therefore, if the membrane were freely permeable to Ca2+, the voltage inside the cell would then approach +120 mV.

Compare the action potential in the TTX-treated contractile cell of Fig. 6 to the nodal cells in Fig. 5. The slow phase 0 and lack of overshoot in the nodal cells is due to the fact that fast sodium channels are not expressed in these cells. The action potential in nodal tissue is maintained entirely by the L-type calcium channels. As expected, TTX has no effect on the action potential in nodal cells.

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