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Autonomic Nerves Modulate Pacemaker Activity

Autonomic Nerves Modulate Pacemaker Activity

FIGURE 12 Effects of catecholamines on SA nodal cells. The catecholamines epinephrine and norepinephrine increase the rate of rise of the pacemaker potential so that it takes a shorter time for the pacemaker potential to reach threshold. Consequently, the interval between action potentials is decreased, increasing the heart rate. (Modified from Katz AM. Physiology of the heart. New York: Raven Press, 1992.)

FIGURE 12 Effects of catecholamines on SA nodal cells. The catecholamines epinephrine and norepinephrine increase the rate of rise of the pacemaker potential so that it takes a shorter time for the pacemaker potential to reach threshold. Consequently, the interval between action potentials is decreased, increasing the heart rate. (Modified from Katz AM. Physiology of the heart. New York: Raven Press, 1992.)

The increase in K+ conductance hyperpolarizes the cell so that it takes a longer time to reach threshold. ACh also slows the rate of rise of the pacemaker potential itself. Both of the preceding effects tend to decrease the firing rate. If the vagus nerve is intensely stimulated, the cells in the SA node will be so hyperpolarized that the pacemaker potential will not reach threshold to fire the cells and the heart will stop beating. After a short time, however, the heart will resume beating with escape beats. The escape rate is much slower because the latent pacemakers in the AV node or the Purkinje network have now taken control.

Catecholamines from the sympathetic nerves increase the heart rate. The dashed line in Fig. 12 shows a recording made after the addition of a catecholamine. Note that the catecholamine increases the rate at which the pacemaker potential approaches threshold. The ionic mechanism causing this increased slope in the pacemaker potential is thought to be an increased Na+ conductance. For many years the channels responsible for this current were not fully characterized and so the current became known as the ''funny'' current, If. It is now thought that If occcurs through the hyperpolari-zing-activated cyclic nucleotide-gated cation channel (HCN).

Transmitter substances of the autonomic nervous system also affect the cell-to-cell conduction velocity in both the atria and the ventricles. ACh slows the rate of propagation, and catecholamines increase the rate of propagation. Intense vagal stimulation can easily depress conduction through the AV node to the point at which conduction to the ventricle fails, a condition called heart block. The ionic mechanisms that underlie these changes in propagation velocity are still not well understood.

Suggested Readings

Katz AM. Physiology of the heart. Philadelphia: Lippincott Williams & Williams, 2001.

Sperelakis N, ed. Heart physiology and pathophysiology. London: Academic Press, 2001

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