214
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
Essential hypertension is related to hered-
ity, age, race, and socioeconom ic status. The
strong hereditary correlation may be related
to genetic abnormalities in renal function
and neurohumoral control mechanisms. The
incidence of essential hypertension increases
with age, and people of African descent are
more likely to develop hypertension than are
Caucasians. Hypertension is more prevalent
among lower socioeconom ic groups.
Some
patients
with
essential
hyperten-
sion are more strongly influenced by stressful
conditions than are normotensive individu-
als. Stress not only leads to acute elevations in
arterial pressure, but it can also lead to chronic
elevations in pressure. Stress activates the sym-
pathetic nervous system, which increases car-
diac output and systemic vascular resistance.
Furthermore, stress causes the adrenal medulla
to secrete more catecholamines (epinephrine
and norepinephrine) than normal. Sympathetic
activation increases circulating angiotensin II,
aldosterone, and vasopressin, which together
can increase systemic vascular resistance and,
through their renal effects, increase sodium
and water retention. In addition, prolonged
elevation of angiotensin II and catecholamines
leads to vascular and cardiac hypertrophy.
Secondary Hypertension
Secondary
hypertension
accounts
for
5%
to 10% of hypertensive cases. This form of
hypertension has identifiable causes that often
can be remedied. Regardless of the underly-
ing cause, arterial pressure becomes elevated
through an increase in cardiac output, an
increase in systemic vascular resistance, or
both. W hen cardiac output is elevated, it is
often related to increased blood volume and
neurohumoral activation of the heart. Several
causes of secondary hypertension are summa-
rized in Table 9-3 and discussed below.
Renal artery stenosis occurs when the renal
artery becomes narrowed (stenotic) owing
to atherosclerotic or fibromuscular lesions.
This reduces the pressure at the afferent arte-
riole, which stimulates the release of renin
by the kidney (see Chapter 6). Increased
plasma renin activity increases circulating
angiotensin II and aldosterone. Angiotensin II
causes vasoconstriction by binding to vascu-
lar AT1 receptors and by augmenting sympa-
thetic influences. Furthermore, angiotensin II
along with aldosterone increases renal sodium
and water reabsorption. The net effect of the
renal actions is an increase in blood volume
that augments cardiac output by the Frank-
Starling mechanism. In addition, chronic ele-
vation of angiotensin II promotes cardiac and
vascular hypertrophy.
Therefore, hyperten-
sion caused by renal artery stenosis is asso-
ciated with increases in cardiac output and
systemic vascular resistance.
Renal disease (e.g., diabetic nephropathy,
glomerulonephritis) damages nephrons in the
kidney. W hen this occurs, the kidney cannot
excrete normal amounts of sodium, and the
pressure natriuresis curve shifts to the right,
which leads to sodium and water retention,
increased blood volume, and increased car-
diac output. Renal disease may increase the
release of renin, leading to a renin-dependent
form of hypertension. The elevation in arte-
rial pressure secondary to renal disease can
be viewed as an attempt by the kidney to
increase renal perfusion, thereby restoring
normal
glomerular
filtration
and
sodium
excretion.
Primary hyperaldosteronism is increased
secretion of aldosterone by an adrenal ade-
noma or adrenal hyperplasia. This condition
causes renal retention of sodium and water,
thereby increasing blood volume and arterial
pressure. Aldosterone acts upon the distal
convoluted tubule and cortical collecting duct
of the kidney to increase sodium reabsorption
in exchange for potassium and hydrogen ion,
which are excreted in the urine. Plasma renin
levels generally are decreased as the body
attempts to suppress the renin-angiotensin
system. In addition, hypokalemia is associ-
ated with the high levels of aldosterone.
A pheochrom ocytoma (a catecholamine-
secreting
tumor,
usually
in
the
adrenal
medulla) can cause high levels of circulating
catecholamines
(both
epinephrine
and
norepinephrine).
A
pheochromocytoma
is
diagnosed by measuring plasma or urine
catecholamine levels and their metabolites
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