208
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
Blood Loss
I
+
i Central Venous
Pressure
I
i
Stroke
Volume
I
i Cardiac
+
Output
+
+
t Systemic Vascular
Resistance
t Venous
Tone
I Arterial
Pressure
I
i Baroreceptor
Firing
t Sympathetic
i Parasympathetic
/
t Heart Rate
and
t Contractility
■ FIGURE 9.5 Activation of baroreceptor mechanisms following acute blood loss (hemorrhage). Blood
loss reduces central venous pressure (cardiac preload), which decreases cardiac output and arterial pres-
sure. Reduced firing of arterial baroreceptors activates the sym pathetic nervous system, which stimulates
cardiac function, and constricts resistance and capacitance vessels. These actions help to elevate (+) the
reduced central venous pressure, stroke volume, cardiac output, and arterial pressure, and thereby help to
restore arterial pressure.
renal mechanisms (Fig. 9.6). Some of these
humoral systems also reinforce the barorecep-
tor reflex by causing cardiac stimulation and
vasoconstriction.
The renin-angiotensin-aldosterone system
is activated by increased renal sympathetic
nerve activity and renal artery hypotension
via decreased sodium delivery to the macula
densa, which releases renin leading to the
formation of angiotensin II (see Chapter 6).
Increased circulating angiotensin II constricts
the systemic vasculature directly by binding
to AT1 receptors and indirectly by enhancing
sympathetic effects. Angiotensin II stimulates
aldosterone
secretion.
Vasopressin
secre-
tion is stimulated by reduced atrial stretch,
sympathetic stimulation, and angiotensin II.
Working together, angiotensin II, aldosterone,
and vasopressin cause the kidneys to retain
sodium and water, thereby increasing blood
volume, cardiac preload and cardiac output.
Increased vasopressin also stimulates thirst
so that more fluid is ingested. The renal and
vascular responses to these hormones are fur-
ther enhanced by decreased secretion of atrial
natriuretic peptide by the atria, resulting from
decreased atrial stretch associated with the
hypovolemic state.
The vascular responses to angiotensin II
and vasopressin occur rapidly in response
to increased plasma concentrations of these
vasoconstrictors. The renal effects of angioten-
sin II, aldosterone, and vasopressin, in contrast,
occur more slowly as decreased sodium and
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