CHAPTER 9 • CARDIOVASCULAR INTEGRATION, ADAPTATION, AND PATHOPHYSIOLOGY
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(vanillylmandelic acid and metanephrine).
This
condition
leads
to
a-adrenoceptor-
mediated
systemic
vasoconstriction
and
P^adrenoceptor-mediated
cardiac
stimula-
tion that can cause substantial elevations in
arterial pressure. Although arterial pressure
rises to very high levels, tachycardia still
occurs because of the direct effects of the
catecholamines on the heart and vasculature.
Excessive P1-adrenoceptor stimulation in the
heart often leads to arrhythmias in addition to
the hypertension.
Aortic coarctation is a narrowing of the
aortic arch usually just distal to the left sub-
clavian artery. It is a congenital defect that
obstructs aortic outflow, leading to elevated
pressures proximal to the coarctation (i.e., ele-
vated arterial pressures in the head and arms).
Distal pressures, however, are not necessarily
reduced as would be expected from the hem o-
dynamics associated with a stenosis. The rea-
son for this is that reduced systemic blood
flow, and in particular reduced renal blood
flow, leads to an increase in the release of renin
and an activation of the renin-angiotensin-
aldosterone system.
This in
turn
elevates
blood volume and arterial pressure. Although
the aortic arch and carotid sinus barorecep-
tors are exposed to higher-than-normal pres-
sures, the baroreceptor reflex is blunted owing
to structural changes in the walls of vessels
where the baroreceptors are located. Further-
more, baroreceptors become desensitized to
chronic elevation in pressure and become
“reset” to the higher pressure.
Preeclampsia is a type of hypertension that
occurs in about 5% of pregnancies during late
second
and third
trimesters.
Preeclampsia
differs from less severe forms of pregnancy-
induced hypertension (gestational hyperten-
sion) in that preeclampsia is associated with a
loss of albumin in the urine because of renal
damage, and pulmonary and systemic edema.
Preeclampsia is also associated with increased
vascular responsiveness to vasoconstrictors,
which can lead to vasospasm. It is unclear
why some women develop this condition dur-
ing pregnancy; however, it usually disappears
after parturition unless an underlying hyper-
tensive condition exists.
Hyperthyroidism induces systemic vaso-
constriction, an increase in blood volume,
and increased cardiac activity, all of which
can lead to hypertension. It is less clear why
some
patients
with
hypothyroidism
also
develop hypertension, but it may be related
to decreased tissue metabolism reducing the
release of vasodilator metabolites,
thereby
producing
vasoconstriction
and
increased
systemic vascular resistance.
Cushing syndrome, which results from
excessive glucocorticoid secretion, can lead to
hypertension. Glucocorticoids such as corti-
sol, which are secreted by the adrenal cortex,
share some of the same physiologic proper-
ties as aldosterone, a mineralocorticoid also
secreted by the adrenal cortex. Therefore,
excessive glucocorticoids can lead to volume
expansion and hypertension.
Sleep apnea is a disorder in w hich peo-
ple repeatedly stop breathing for short peri-
ods of time (10 to 30 seconds) during their
sleep; this can occur dozens of times per
hour. Breathing is m ost com m only inter-
rupted by airway obstruction, and less com -
m only by disorders of the central nervous
system. This condition is often associated
with
obesity.
Individuals
suffering
from
sleep
apnea
have
a higher
incidence
of
hypertension. The mechanism of hyperten-
sion may be related to sympathetic activa-
tion and hormonal changes associated with
repeated periods of apnea-induced hypoxia
and hypercapnia, and from stress associated
with the loss of sleep.
Physiologic Basis for Therapeutic
Intervention
If a person has secondary hypertension, it is
sometimes possible to correct the underlying
cause. For example, renal artery stenosis can
be corrected by placing a wire stent within the
renal artery to maintain vessel patency; aortic
coarctation can be surgically corrected; a phe-
ochromocytoma can be removed. However,
for the majority of people who have essential
hypertension, the cause is unknown, so it
cannot be targeted for correction. Therefore,
the therapeutic approach for these patients
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