Ganong's Review of Medical Physiology, 23rd Edition

358 SECTION IV Endocrine & Reproductive Physiology
8
20
Change in
17-hydroxy-
6
15
corticoid
(μg/min)
4
10
2
5
0
0.042 0.083 0.167 0.42 1.67
Dose of angiotensin II
(μg/min)
0
No. of dogs (5)* (2) (8) (7) (7)
*Aldosterone values in 3 dogs
Change in
aldosterone
output
(ng/min)
FIGURE 22–24 Changes in adrenal venous output of
steroids produced by angiotensin II in nephrectomized
hypophysectomized dogs.
renin–angiotensin system in a feedback fashion (Figure 22–25).
A drop in ECF volume or intra-arterial vascular volume leads to
a reflex increase in renal nerve discharge and decreases renal
arterial pressure. Both changes increase renin secretion, and the
angiotensin II formed by the action of the renin increases the
rate of secretion of aldosterone. The aldosterone causes Na +
and, secondarily, water retention, expanding ECF volume and
shutting off the stimulus that initiated increased renin secretion.
Hemorrhage stimulates ACTH and renin secretion. Like
hemorrhage, standing and constriction of the thoracic inferior
vena cava decrease intrarenal arterial pressure. Dietary sodium
restriction also increases aldosterone secretion via the renin–
angiotensin system (Figure 22–26). Such restriction reduces
ECF volume, but aldosterone and renin secretion are increased
before any consistent decrease in blood pressure takes place.
Consequently, the initial increase in renin secretion produced
by dietary sodium restriction is probably due to a reflex
increase in the activity of the renal nerves. The increase in cir-
25
Juxtaglomerular
apparatus
Angiotensinogen
Angiotensin I
Angiotensin II
Adrenal
cortex
Renin
Angiotensinconverting
enzyme
culating angiotensin II produced by salt depletion upregulates
the angiotensin II receptors in the adrenal cortex and hence
increases the response to angiotensin II, whereas it down-regulates
the angiotensin II receptors in the blood vessels.
ELECTROLYTES & OTHER FACTORS
An acute decline in plasma Na + of about 20 mEq/L stimulates
aldosterone secretion, but changes of this magnitude are rare.
However, the plasma K + level need increase only 1 mEq/L to
stimulate aldosterone secretion, and transient increases of this
magnitude may occur after a meal, particularly if it is rich in
K + . Like angiotensin II, K + stimulates the conversion of cholesterol
to pregnenolone and the conversion of deoxycorticosterone
to aldosterone. It appears to act by depolarizing the cell,
which opens voltage-gated Ca 2+ channels, increasing intracellular
Ca 2+ . The sensitivity of the zona glomerulosa to angiotensin
II and consequently to a low-sodium diet is
decreased by a low-potassium diet.
In normal individuals, plasma aldosterone concentrations
increase during the portion of the day that the individual is
carrying on activities in the upright position. This increase is
due to a decrease in the rate of removal of aldosterone from
the circulation by the liver and an increase in aldosterone
secretion due to a postural increase in renin secretion. Individuals
who are confined to bed show a circadian rhythm of
aldosterone and renin secretion, with the highest values in the
early morning before awakening.
Atrial natriuretic peptide (ANP) inhibits renin secretion
and decreases the responsiveness of the zona glomerulosa to
angiotensin II (see Chapter 39).
The mechanisms by which ACTH, angiotensin II, and K +
stimulate aldosterone secretion are summarized in Table 22–7.
Increased renal arterial
mean pressure, decreased
discharge of renal nerves
Increased extracellular
fluid volume
Aldosterone Decreased Na +
(and water) excretion
FIGURE 22–25 Feedback mechanism regulating aldosterone secretion. The dashed arrow indicates inhibiition.