Chapter 14
the synthesis of all the channels and pumps shown in the cor-
tical collecting duct. By this same mechanism, aldosterone
also stimulates sodium absorption from the lumens of both
the large intestine and the ducts carrying fl uid from the sweat
glands and salivary glands. In this manner, less sodium is lost
in the feces and from the surface of the skin in sweat.
When a person eats a diet high in sodium, aldosterone
secretion is low, whereas it is high when the person ingests a
low-sodium diet or becomes sodium-depleted for some other
reason. What controls the secretion of aldosterone under these
circumstances? The answer is the hormone angiotensin II,
which acts directly on the adrenal cortex to stimulate the secre-
tion of aldosterone.
Angiotensin II
is a component of the hormonal com-
plex termed the
renin-angiotensin system,
summarized in
Figure 14–21
(pronounced REE-nin) is an enzyme
secreted by the juxtaglomerular cells of the juxtaglomeru-
lar apparatuses in the kidneys. Once in the bloodstream,
renin splits a small polypeptide,
angiotensin I,
from a large
plasma protein,
which is produced by
the liver. Angiotensin I, a biologically inactive peptide, then
undergoes further cleavage to form the active agent of the
renin-angiotensin system, angiotensin II. This conversion is
mediated by an enzyme known as
enzyme (ACE),
which is found in very high concentration on
the luminal surface of capillary endothelial cells. Angiotensin
II exerts many effects, but the most important are the stimu-
lation of the secretion of aldosterone and the constriction of
arterioles (described in Chapter 12). Plasma angiotensin II is
high during salt depletion and low when salt intake is high. It
is this change in angiotensin II that brings about the changes
in aldosterone secretion.
What causes the changes in plasma angiotensin II con-
centration with changes in salt balance? Angiotensinogen and
angiotensin-converting enzyme are usually present in excess,
so the rate-limiting factor in angiotensin II formation is the
plasma renin concentration. Thus, the chain of events in salt
depletion is increased renin secretion
increased plasma
renin concentration
increased plasma angiotensin I concen-
increased plasma angiotensin II concentration
increased aldosterone release
increased plasma aldosterone
What are the mechanisms by which sodium depletion
causes an increase in renin secretion (
Figure 14–22
)? There
are at least three distinct inputs to the juxtaglomerular cells:
(1) the renal sympathetic nerves, (2) intrarenal baroreceptors,
and (3) the macula densa.
The renal sympathetic nerves directly innervate the juxta-
glomerular cells, and an increase in the activity of these nerves
stimulates renin secretion. This makes sense because these
nerves are refl exly activated via baroreceptors whenever a
reduction in body sodium (and, therefore, plasma volume)
lowers cardiovascular pressures (see Figure 14–20).
The other two inputs for controlling renin release—
intrarenal baroreceptors and the macula densa—are contained
within the kidneys and require no external neuroendocrine
input (although such input can infl uence them). As noted ear-
lier, the juxtaglomerular cells are located in the walls of the
afferent arterioles. They are sensitive to the pressure within
these arterioles, and so function as
intrarenal baroreceptors.
When blood pressure in the kidneys decreases, as occurs when
plasma volume is decreased, these cells are stretched less and,
therefore, secrete more renin (see Figure 14–22). Thus, the
juxtaglomerular cells respond simultaneously to the combined
effects of sympathetic input, triggered by baroreceptors exter-
nal to the kidneys, and to their own pressure sensitivity.
Angiotensin I
(10 aa)
Angiotensin II
(8 aa)
Renin (enzyme)
(453 aa)
Stimuli to renin
Angiotensin I
Angiotensin II
Blood pressure
Salt and H
Figure 14–21
Summary of the renin-angiotensin system and the stimulation of
aldosterone secretion by angiotensin II. Angiotensin-converting
enzyme is located on the surface of capillary endothelial cells. The
plasma concentration of renin is the rate-limiting factor in the renin-
angiotensin system; that is, it is the major determinant of the plasma
concentration of angiotensin II.
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