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Chapter 12
Other Baroreceptors
The large systemic veins, the pulmonary vessels, and the walls
of the heart also contain baroreceptors, most of which function
in a manner analogous to the arterial baroreceptors. By keep-
ing brain cardiovascular control centers constantly informed
about changes in the systemic venous, pulmonary, atrial, and
ventricular pressures, these other baroreceptors provide a
further degree of regulatory sensitivity. In essence, they con-
tribute a feedforward component of arterial pressure control.
For example, a slight decrease in ventricular pressure refl exly
increases the activity of the sympathetic nervous system even
before the change lowers cardiac output and arterial pressure
far enough for the arterial baroreceptors to detect it.
Blood Volume and Long-Term
Regulation of Arterial Pressure
The fact that the arterial baroreceptors (and other barorecep-
tors as well) adapt to prolonged changes in pressure means that
the baroreceptor refl exes cannot set long-term arterial pres-
sure. The major mechanism for long-term regulation occurs
through the blood volume. As described earlier, blood volume
is a major determinant of arterial pressure because it infl u-
ences, in turn, venous pressure, venous return, end-diastolic
volume, stroke volume, and cardiac output. Thus, increased
blood volume increases arterial pressure. But the opposite
causal chain also exists—an increased arterial pressure reduces
Arterial pressure
(toward normal)
Total peripheral resistance
Cardiac output
(toward normal)
Venous pressure
(toward normal)
Venous return
(toward normal)
End-diastolic
volume
(toward normal)
Sympathetic
discharge
to arterioles
Sympathetic
discharge
to heart
Sympathetic
discharge
to veins
Parasympathetic
discharge
to heart
Firing by arterial
baroreceptors
Arterial pressure
(see Fig. 12-52)
Hemorrhage
Cardiac muscle
Stroke volume
(toward normal)
Veins
Constriction
SA node
Heart rate
Arterioles
Constriction
Begin
Figure 12–56
Arterial baroreceptor refl ex compensation for
hemorrhage. The compensatory mechanisms do not
restore arterial pressure completely to normal. The
increases designated “toward normal” are relative to
prehemorrhage values; for example, the stroke volume
is increased refl exly “toward normal” relative to the
low point caused by the hemorrhage (i.e., before the
refl ex occurs), but it does not reach the level it had
prior to the hemorrhage. For simplicity, the fact that
plasma angiotensin II and vasopressin are also refl exly
increased and help constrict arterioles is not shown.
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