CARDIOVASCULAR PHYSIOLOGY CONCEPTS
endothelium, particularly in the lungs, has
an enzyme, angiotensin-converting enzyme
(ACE), that cleaves off two amino acids to
form the octapeptide, angiotensin II.
angiotensin II receptors (AT1) (Fig. 6.11).
1. Constricts resistance vessels, thereby increas-
ing systemic vascular resistance and arterial
2. Enhances sympathetic adrenergic activ-
ity by facilitating norepinephrine release
from sympathetic nerve endings, inhibit-
ing norepinephrine reuptake by nerve end-
ings, and by binding to AT1
receptors in the
RVLM, which increases sympathetic effer-
3. Acts upon the adrenal cortex to release
aldosterone, which in turn acts upon the
kidneys to increase sodium and fluid reten-
tion, thereby increasing blood volume.
4. Stimulates the release of vasopressin from
the posterior pituitary, which acts upon
the kidneys to increase fluid retention and
5. Stimulates thirst centers within the brain,
which can lead to an increase in blood
6. Stimulates cardiac and vascular hypertrophy.
Angiotensin II is continuously produced under
change under different physiologic conditions.
For example, when a person exercises, circulat-
ing levels of angiotensin II increase. An increase
in renin release during exercise probably results
from sympathetic stimulation of the kidneys.
Changes in body posture likewise alter circulat-
ing AII levels, which are increased when a per-
son stands. As with exercise, this results from
sympathetic activation. Dehydration and loss
of blood volume (hypovolemia) stimulate renin
release and angiotensin II formation in response
to renal artery hypotension, decreased glomeru-
lar filtration rate, and sympathetic activation.
associated with changes in circulating angio-
tensin II and aldosterone. For example, second-
ary hypertension caused by renal artery stenosis
is associated with increased renin release and
Sodium & Fluid
■ FIGURE 6.11 Form ation of angiotensin II and its effects on renal, vascular, and cardiac function. Renin is
released by the kidneys in response to sym pathetic stim ulation, hypotension, and decreased sodium deliv-
ery to distal tubules. Renin acts upon angiotensinogen to form angiotensin I
which is converted to
angiotensin II (AII) by angiotensin-converting enzyme (ACE). AII has several im portant actions: stimulates
aldosterone release, which increases renal sodium reabsorption; directly stimulates renal sodium reab-
sorption; stimulates thirst; stimulates release of antidiuretic hormone (ADH); produces systemic vaso-
constriction; activates the sym pathetic nervous system; and causes cardiac and vascular sm ooth muscle
hypertrophy. The overall systemic effect of increased AII is increased blood volume, venous pressure, and