Page 753 - Fundamentals of anatomy physiology
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740 Unit 4 Fluids and Transport
Figure 20–22 Autonomic Regulation of Pacemaker Function. cutting the vagus nerves increases the heart rate, and
sympathetic blocking agents slow the heart rate.
+20 Normal (resting) Spontaneous
depolarization Parasympathetic effects dominate in a healthy,
Membrane 0 resting individual. Without autonomic innervation,
potential the pacemaker cells of the SA node establish the heart
(mV) rate. Such a heart beats at a rate of 80–100 bpm. At
–30 rest, a typical adult heart with normal innervation
Threshold beats more slowly, at 70–80 bpm, due to activity in
the parasympathetic nerves innervating the SA node.
–60 If parasympathetic activity increases, the heart rate
Heart rate: 75 bpm declines further. Conversely, the heart rate increases if
parasympathetic activity decreases, or if sympathetic
0.8 1.6 2.4 activation occurs. Through dual innervation and ad-
justments in autonomic tone, the ANS can make very
a Pacemaker cells have membrane potentials closer to delicate adjustments in cardiovascular function to
threshold than those of other cardiac muscle cells (–60 mV meet the demands of other systems.
versus –90 mV). Their plasma membranes undergo
spontaneous depolarization to threshold, producing action Effects on the SA Node. How do the sympathetic
potentials at a frequency determined by (1) the membrane and parasympathetic divisions alter the heart rate?
potential and (2) the rate of depolarization. They do so by changing the ionic permeabilities of
cells in the conducting system. The most dramatic ef-
+20 Parasympathetic stimulation fects take place at the SA node, which affects the heart
Hyperpolarization rate through changes in the rate at which impulses
Membrane 0 are generated.
potential
Consider the SA node of a resting individual
(mV) whose heart is beating at 75 bpm (Figure 20–22a).
Any factor that changes the rate of spontaneous depo-
–30 larization or the duration of repolarization in nodal
cells will alter the heart rate by changing the time
Threshold required for these cells to reach threshold. Acetyl-
choline released by parasympathetic neurons opens
–60 chemically gated K+ channels in the plasma mem-
brane. Then K+ leaves the nodal cells, dramatically
Heart rate: 40 bpm Slower depolarization slowing their rate of spontaneous depolarization and
also slightly extending their duration of repolariza-
20 0.8 1.6 2.4 tion (Figure 20–22b). As a result, heart rate declines.
b Parasympathetic stimulation releases ACh, which extends Norepinephrine released by sympathetic neu-
repolarization and decreases the rate of spontaneous rons binds to beta-1 receptors, leading to the opening
depolarization. The heart rate slows. of sodium ion channels and calcium ion channels.
Then an influx of positively charged ions increases
+20 Sympathetic stimulation the rate of depolarization and shortens the period of
repolarization. The nodal cells reach threshold more
Membrane 0 Reduced repolarization quickly, and the heart rate increases (Figure 20–22c).
potential Heart rate: 120 bpm
(mV)
–30
Threshold
–60 More rapid
depolarization
0.8 1.6 2.4
Time (sec)
c Sympathetic stimulation releases NE, which shortens The Atrial Reflex. The atrial reflex, or Bainbridge
repolarization and accelerates the rate of spontaneous reflex, involves adjustments in heart rate in response
depolarization. As a result, the heart rate increases. to an increase in the venous return (the amount of
blood returning to the heart through veins). When
the walls of the right atrium are stretched, stretch
Autonomic Tone. Like other organs with dual innervation, the receptors there trigger a reflexive increase in heart rate by stimu-
heart has a resting autonomic tone. Both autonomic divisions lating sympathetic activity (Figure 20–22). Thus, when the rate
are normally active at a steady background level, releasing ACh of venous return to the heart increases, so does the heart rate,
and NE at the nodes and into the myocardium. For this reason, and for this reason the cardiac output increases as well.

