activated. In combination, this results in slow depolarization of the myocyte. If the membrane potential depolarizes above the threshold for the opening of ICa++, an action potential is generated.

Myocytes within the sinoatrial node possess the most rapid intrinsic rate of automaticity; therefore, the sinoatrial node serves as the normal pacemaker of the heart. Specialized cells within the atria, atrioventricular (A-V) node, and His-Purkinje system are capable of spontaneous depolarization, albeit at a slower rate. The more rapid rate of depolarization of the sinoatrial nodal cells normally suppresses all of the other cells with the potential for automaticity. The other cells will become pacemakers when their own intrinsic rate of depolarization becomes greater than that of the sinoatrial node or when the pacemaker cells within the sinoatrial node are depressed. When impulses fail to conduct across the A-V node to excite the ventricular myocardium (heart block), spontaneous depolarization within the His-Purkinje system may become the dominant pacemaker maintaining cardiac rhythm and cardiac output.

The rate of pacemaker discharge within these specialized myocytes is influenced by the activity of both divisions of the autonomic nervous system. Increased sympathetic nerve activity to the heart, the release of catecholamines from the adrenal medulla, or the exogenous administration of adrenomimetic amines will cause an increase in the rate of pacemaker activity through stimulation of p-adrenoceptors on the pacemaker cells (Figure 16.3).

The parasympathetic nervous system, through the vagus nerve, inhibits the spontaneous rate of depolarization of pacemaker cells. The release of acetylcholine from cholinergic vagal fibers increases potassium conductance (gK+) in pacemaker cells, and this enhanced outward movement of K+ results in a more negative po

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