Page 207 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

!
an AP. The slope of their APs therefore rises nephrine (E). NE and E bind with ! 1-adreno-
more sharply than that of a pacemaker poten- ceptors (! p. 84ff.). The firing frequency of the
tial (! A). A resting potential prevails between SA node is increased by NE and E (positive
APs, i.e. spontaneous depolarization normally chronotropism) and decreased by ACh (nega-
does not occur in the working myocardium. tive chronotropism) because these substances
The long-lasting myocardial AP has a charac- alter the slopes of the PP and the MDP in the SA
teristic plateau (! p. 59 A). Thus, the first- cells (! B3a and c). Under the influence of ACh,
stimulated parts of the myocardium are still in the slope of the PP becomes flatter and the
a refractory state when the AP reaches the last- MDP becomes more negative g K rises. In
stimulated parts of the myocardium. This pre- versely, slope and amplitude of PP rises under
vents the cyclic re-entry of APs in the myo- the influence of E or sympathetic stimuli
+
cardium. This holds true, regardless of (higher I f ) due to a rise in cation (Na ) conduct-
whether the heart rate is very fast or very slow ance and, under certain conditions, a decrease
Cardiovascular System gated Ca 2+ 2+ 2+ conduction system. This is decisive when the
in the g K. Only NE and E have chronotropic ef-
since the duration of an AP varies according to
heart rate (! B2).
fects in the lesser components of the impulse
Role of Ca . The incoming AP opens voltage-
AV node or tertiary pacemakers take over.
channels (associated with dihy-
dropyridine receptors) on the sarcolemma of
ACh (left branch of vagus nerve) decreases
myocardial cells, starting an influx of Ca from
the velocity of impulse conduction in the AV
the ECF (! p. 63/B3). This produces a local in-
node, whereas NE and E increase it due to their
2+
2+
spectively. This is mainly achieved through
turn, triggers the opening of ligand-gated, ry-
8 crease in cytosolic Ca (Ca “spark”) which, in negative and positive dromotropic effects, re-
anodine-sensitive Ca
changes in the amplitude and slope of the up-
channels in the sarco-
2+
plasmic reticulum (Ca 2+ store). The influx of stroke of the AP (! B3c and B4), g K and g Ca.
2+
Ca into the cytosol results in electromechani- In positive inotropism, NE and E have a
cal coupling (! p. 62) and myocardial contrac- direct effect on the working myocardium. The
tion. The cytosolic Ca 2+ is also determined by resulting increase in contractility is based on
active transport of Ca 2+ ions back (a) into the an increased influx of Ca 2+ ions from the ECF
2+
Ca 2+ stores via a Ca -ATPase, called SERCA, triggered by ! 1-adrenoceptors, resulting in an
which is stimulated by phospholamban, and increased cytosolic Ca . This Ca influx can be
2+
2+
2+
(b) to the ECF. This is achieved with the aid of a inhibited by administering Ca channel block-
2+
+
Ca -ATPase and a 3 Na /Ca 2+ exchange carrier ers (Ca 2+ antagonists). Other factors that in-
that is driven by the electrochemical Na + crease cardiac contractility are an increase in
+
+
gradient established by Na -K -ATPase. AP duration, resulting in a longer duration of
+
+
Although the heart beats autonomously, Ca 2+ influx, and inhibition of Na -K -ATPase
efferent cardiac nerves are mainly responsible (e.g., by the cardiac glycosides digitalis and
for modulating heart action according to strophanthin). The consequences are: flatter
+
changing needs. The autonomic nervous system Na gradient across the cell membrane !
+
(and epinephrine in plasma) can alter the fol- decreased driving force for 3 Na /Ca 2+ ex-
lowing aspects of heart action: (a) rate of im- change carriers ! decreased Ca 2+ efflux ! in-
pulse generation by the pacemaker and, thus, creased cytosolic Ca 2+ conc.
the heart rate (chronotropism); (b) velocity of When the heart rate is low, Ca 2+ influx over
impulse conduction, especially in the AV node time is also low (fewer APs per unit time), al-
(dromotropism); and (c) contractility of the lowing plenty of time for the efflux of Ca 2+ be-
heart, i.e., the force of cardiac muscle contrac- tween APs. The mean cytosolic Ca 2+ conc. is
tion at a given initial fiber length (inotropism). therefore reduced and contractility is low.
These changes in heart action are induced Only by this indirect mechanism are parasym-
by acetylcholine (ACh; ! p. 82) released by pathetic neurons able to elicit a negative in-
parasympathetic fibers of the vagus nerve otropic effect (frequency inotropism). NE and E
(binds with M 2 cholinoceptors on pacemaker can exert their positive inotropic effects either
194 cells), by norepinephrine (NE) released by indirectly by increasing the high heart or
sympathetic nerve fibers, and by plasma epi- directly via ! 1-adrenoceptors of the working
myocardium.
Despopoulos, Color Atlas of Physiology © 2003 Thieme
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