Purkinje cells are similar to atrial and ventricular cells in that they generate an action potential with a fast upstroke due to the activity of sodium channels. However, unlike atrial and ventricular cells, the membrane potential during phase 4 exhibits spontaneous depolarization. This is due to the presence of pacemaker channels that generate an inward depolarizing pacemaker current. This is sometimes referred to as the “funny” current (If), because the channels involved have the unusual property of being activated by membrane hyperpolarization. Under some circumstances, Purkinje cells can act as pacemakers for the heart by spontaneously depolarizing and initiating an action potential that is then propagated throughout the ventricular myocardium. However, under normal conditions, the action potential in Purkinje cells is triggered by impulses that originate in the SA node and are conducted to these cells through the AV node.
Pacemaking activity in the SA node is due to spontaneous depolarization during phase 4 of the action potential as well (Figure 14–1). This diastolic depolarization is mediated in part by the activity of pacemaker channels. It is also thought to be due to the net inward current generated by the sodium-calcium exchanger, which is activated by the spontaneous release of calcium from intracellular storage sites. Unlike the action potential in Purkinje cells, spontaneous depolarization in the SA node triggers the upstroke of an action potential that is primarily due to an increase in permeability to calcium, not sodium. Because the calcium channels involved open or activate slowly, the maximum upstroke velocity of the action potential in SA node cells is relatively slow. Repolarization occurs when the calcium channels subsequently close due to inactivation and delayed rectifier-type potassium channels open.
A similar process is involved in generating action potentials in the AV node. Although the intrinsic rate of spontaneous diastolic depolarization in the AV node is typically faster than that of Purkinje cells, it is still slower than the rate of depolarization in the SA node. Therefore, action potentials in the AV node are normally triggered by impulses that originate in the SA node and are conducted to the AV node through the atria. It is important to recognize that action potential upstroke velocity is a key determinant of impulse conduction velocity. Because the action potential upstroke in AV node cells is mediated by calcium channels, which open or activate relatively slowly, impulse conduction through the AV node is slow. This contributes to the delay between atrial and ventricular contraction.
Electrical activity in the SA node and AV node is significantly influenced by the autonomic nervous system (see Chapter 6). Sympathetic activation of β adrenoceptors speeds pacemaker activity in the SA node and impulse propagation through the AV node by enhancing pacemaker and calcium channel activity, respectively. Conversely, parasympathetic activation of muscarinic receptors slows pacemaker activity and conduction velocity by inhibiting the activity of these channels, as well as by increasing the potassium conductance by turning on acetylcholine-activated potassium channels.
The Effect of Membrane Potential on Excitability