20
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
SA Nodal Cell
■ FIGURE 2.7 Effects of sympathetic and parasympathetic (vagal) stimulation on sinoatrial (SA) nodal pace-
maker activity. Sympathetic stimulation increases the firing rate by increasing the slope of phase 4 and lower-
ing the threshold for the action potential. Vagal stimulation has the opposite effects, and it hyperpolarizes the
cell. Horizontal dashed lines represent threshold and maximal hyperpolarization potentials for normal cell.
activation (see Chapter 3). Acetylcholine also
activates a special type of potassium channel
(KACh channel) that hyperpolarizes the cell by
increasing potassium conductance.
Nonneural mechanisms also alter pacemaker
activity (Table 2-2). For example, circulating
catecholamines (epinephrine and norepineph-
rine) cause tachycardia (abnormally high heart
rate) by a mechanism similar to norepinephrine
TABLE 2-2
FACTORS INCREASING OR
DECREASING THE SA NODE
FIRING RATE
IN C R E A S IN G
| d e c r e a s in g
Sympathetic
stimulation
Parasympathetic
stimulation
Muscarinic receptor
antagonist
Muscarinic receptor
agonists
b-Adrenoceptor
agonists
fi-Blockers
Circulating cat-
echolamines
Ischemia/hypoxia
Hypokalemia
Hyperkalemia
Hyperthyroidism
Sodium and calcium
channel blockers
Hyperthermia
Hypothermia
released by sympathetic nerves. Hyperthyroid-
ism induces tachycardia, and hypothyroidism
induces bradycardia (abnormally low heart
rate). Changes in the serum concentration of
ions, particularly potassium, can cause changes
in SA node firing rate. Hyperkalemia induces
bradycardia or can even stop SA nodal firing,
whereas hypokalemia increases the rate of
phase 4 depolarization and causes tachycar-
dia, apparently by decreasing potassium con-
ductance during phase 4. Cellular hypoxia
depolarizes the membrane potential, causing
bradycardia and abolition of pacemaker activ-
ity Increased body temperature (e.g., fever)
leads to increased rate of SA nodal firing.
Various drugs used to treat abnormal heart
rhythm (i.e., antiarrhythmic drugs) also affect
SA nodal rhythm. Calcium channel blockers,
for example, cause bradycardia by i nhibiting
L-type calcium channels, which reduces slow
inward Ca++ currents during phase 4 and
phase 0. Drugs affecting autonomic control
or autonomic receptors (e.g., P-blockers and
M2 receptor antagonists; P-adrenoceptor ago-
nists) alter pacemaker activity. Digoxin causes
bradycardia by increasing parasympathetic
activity and inhibiting the sarcolemmal Na+/
K+-ATPase, which leads to depolarization.
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