Cardiac Output, Blood Flow, and Blood Pressure 461
Regulation by Aldosterone
From the preceding discussion, it is clear that a certain amount
of dietary salt is required to maintain blood volume and pres-
sure. Since Na^1 and Cl^2 are easily filtered in the kidneys, a
mechanism must exist to promote the reabsorption and reten-
tion of salt when the dietary salt intake is too low. Aldosterone,
a steroid hormone secreted by the adrenal cortex, stimulates
the reabsorption of salt by the kidneys. Aldosterone is thus a
“salt-retaining hormone.” Retention of salt indirectly promotes
retention of water (in part, by the action of ADH, as previously
discussed). The action of aldosterone produces an increase in
blood volume, but, unlike ADH, it does not produce a change
in plasma osmolality. This is because aldosterone promotes
the reabsorption of salt and water in proportionate amounts,
whereas ADH promotes only the reabsorption of water. Thus,
unlike ADH, aldosterone does not act to dilute the blood.
The secretion of aldosterone is stimulated during salt
deprivation, when the blood volume and pressure are reduced.
The adrenal cortex, however, is not directly stimulated to
secrete aldosterone by these conditions. Instead, a decrease in
blood volume and pressure activates an intermediate mecha-
nism, described next.
FITNESS APPLICATION
Hydration during exercise becomes increasingly important
as the exercise is prolonged, because sweating can cause
the loss of a substantial amount of water (up to 900 mL per
hour). Lowered blood volume can lower the cardiac output
and blood flow. Among other effects, this reduces the abil-
ity of the body to dissipate heat and limits the extent of
the exercise. Drinking appropriate amounts of water can
alleviate this, but only if the exercise is not too long and
strenuous. If it is, then electrolytes—primarily Na^1 , K^1 , and
Cl^2 —that are also lost in sweat must be replenished. When
that happens, drinking water may quench thirst (because
the water restores a normal plasma osmolality, satisfying
the osmoreceptors) but not maintain the blood volume.
Sports drinks that contain the proper amount of electro-
lytes and carbohydrates (to help maintain blood glucose
when glycogen reserves are depleted), taken not just when
thirsty but at predetermined intervals, may be better for
long, endurance exercises.
Clinical Investigation CLUES
Mark trained for marathons and experienced dizziness
upon standing. He was told to drink more and to switch
to sports drinks for such prolonged exercise.
- What might have caused Mark’s dizziness?
- How might sports drinks under these circumstances
be better for him than water?
FITNESS APPLICATION
Salt has been highly valued throughout human history
because it is often in short supply, is needed to maintain blood
volume and pressure, and is used for food preservation. For
example, salt cakes were used as money in Abyssinia, and
Roman soldiers were often paid with salt—a practice from
which the word salary (sal 5 salt ) derives, as does the phrase
“worth his salt.” Salt has also played roles in many national
events; for example, Mahatma Gandhi led Indians, in their bid
for independence, to make their own salt in defiance of a Brit-
ish monopoly.
Renin-Angiotensin-Aldosterone System
Salt deprivation results in low blood volume and pressure, as
described in the previous section on ADH. This lowers the
blood pressure in the renal artery and reduces the amount of
NaCl and water in the renal filtrate. The juxtaglomerular appa-
ratus in the kidneys (chapter 17; see fig. 17.26) senses these
changes and, in response, secretes the enzyme renin into
the blood (chapter 17, section 17.5). This enzyme cleaves a
ten-amino-acid polypeptide called angiotensin I from a plasma
protein called angiotensinogen. As angiotensin I passes
through the capillaries of the lungs, an angiotensin-converting
enzyme (ACE) removes two amino acids. This leaves an eight-
amino-acid polypeptide called angiotensin II ( fig. 14.12 ). Con-
ditions of salt deprivation, low blood volume, and low blood
pressure, in summary, cause increased production of angioten-
sin II in the blood. (High blood pressure, by contrast, suppresses
renin secretion and thereby results in reduced production of
angiotensin II.)
Angiotensin II exerts numerous effects that cause blood
pressure to rise. Its most direct effect is to stimulate contraction
of the smooth muscle layers of the small arteries and arterioles.
By this means, angiotensin II is a powerful vasoconstrictor,
increasing the total peripheral resistance and thus the arterial
blood pressure. Angiotensin II also promotes a rise in blood
volume (thereby increasing the blood pressure) by stimulating
(1) the thirst center in the hypothalamus, and (2) the adrenal
cortex to secrete aldosterone.
When the thirst center in the hypothalamus is stimu-
lated, more water is taken into the intestine and then the
blood. When the adrenal cortex is stimulated by angioten-
sin II to secrete more aldosterone, the increased aldosterone
stimulates the kidneys to retain more salt and water. The
relationship between the kidneys, angiotensin II, and aldo-
sterone is described as the renin-angiotensin-aldosterone
system. As a result of thirst and the activation of the renin-
angiotensin-aldosterone system, we drink more, retain more
NaCl, and urinate less (thereby increasing the blood volume)
when conditions of low blood volume and pressure cause an
increased secretion of renin from the juxtaglomerular appa-
ratus of the kidneys.