Cardiovascular Physiology
411
blood volume (more specifi cally, the plasma component of the
blood volume) by increasing the excretion of salt and water by
the kidneys, as will be described in Chapter 14.
Figure 12–57
illustrates how these two causal chains
constitute negative feedback loops that determine both
blood volume and arterial pressure. An increase in blood
pressure, whatever the reason, causes a decrease in blood vol-
ume, which tends to bring the blood pressure back down.
An increase in the blood volume, whatever the reason, raises
the blood pressure, which tends to bring the blood volume
back down. The important point is this: Because arterial pres-
sure infl uences blood volume but blood volume also infl u-
ences arterial pressure, blood pressure can stabilize, in the
long run, only at a value at which blood volume is also sta-
ble. Consequently, changes in steady-state blood volume are
the single most important long-term determinant of blood
pressure.
Other Cardiovascular
Refl exes and Responses
Stimuli acting upon receptors other than baroreceptors can
initiate refl exes that cause changes in arterial pressure. For
example, the following stimuli all cause an increase in blood
pressure: decreased arterial oxygen concentration; increased
arterial carbon dioxide concentration; decreased blood fl ow to
the brain; and pain originating in the skin. In contrast, pain
originating in the viscera or joints may cause
decreases
in arte-
rial pressure.
Many physiological states such as eating and sexual activ-
ity are also associated with changes in blood pressure. For
example, attending a stressful business meeting may raise mean
blood pressure by as much as 20 mmHg, walking increases it
10 mmHg, and sleeping lowers it 10 mmHg. Mood also has a
signifi cant effect on blood pressure, which tends to be lower
when people report that they are happy than when they are
angry or anxious.
These changes are triggered by input from receptors or
higher brain centers to the medullary cardiovascular center
or, in some cases, to pathways distinct from these centers. For
example, the fi bers of certain neurons whose cell bodies are in
the cerebral cortex and hypothalamus synapse directly on the
sympathetic neurons in the spinal cord, bypassing the medul-
lary center altogether.
There is a considerable degree of fl
exibility and integra-
tion in the control of blood pressure. For example, in an exper-
imental animal, electrical stimulation of a discrete area of the
hypothalamus elicits all the usually observed neurally medi-
ated cardiovascular responses to an acute emotional situation.
Stimulation of other brain sites elicits cardiovascular changes
appropriate to the maintenance of body temperature, feeding,
or sleeping. It seems such outputs are “preprogrammed.” The
complete pattern can be triggered by a natural stimulus that
initiates the fl ow of information to the appropriate brain con-
trol center.
Begin
Begin
Plasma volume
Cardiac output
End-diastolic volume
Venous return
Venous pressure
Blood volume
Plasma volume
Arterial pressure
(a)
Cardiac output
End-diastolic volume
Venous return
Venous pressure
Arterial pressure
(b)
Blood volume
Cardiac muscle
Stroke volume
Kidneys
Urinary loss of
sodium and water
Kidneys
Urinary loss of
sodium and water
Cardiac muscle
Stroke volume
––
Figure 12–57
Causal reciprocal relationships between arterial pressure and blood volume. (a) An increase in arterial pressure due, for example, to an increased
cardiac output induces a decrease in blood volume by promoting fl uid excretion by the kidneys. This tends to restore arterial pressure to its
original value. (b) An increase in blood volume due, for example, to increased fl uid ingestion induces an increase in arterial pressure, which
tends to restore blood volume to its original value by promoting fl uid excretion by the kidneys. Because of these relationships, blood volume is
a major determinant of arterial pressure.
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