588
UNIT FOUR
H
ypertension, or high blood pressure, is
persistently elevated arterial pressure.
It is one of the more common diseases
of the cardiovascular system in industrialized
nations.
High blood pressure with unknown cause
is called
essential
(also primary or idiopathic)
hypertension.
Elevated blood pressure that is a
consequence of another problem, such as arte-
riosclerosis or kidney disease, is called secondary
hypertension.
Arteriosclerosis is accompanied by decreased
elasticity of the arterial walls and narrowed ves-
sel lumens, which raise blood pressure. Kidney
diseases often produce changes that interfere
with blood F
ow to kidney cells. In response, the
affected tissues may release an enzyme called
renin
that leads to the production of
angiotensin
II,
a powerful vasoconstrictor that increases
peripheral resistance in the arterial system, rais-
ing arterial pressure (±
g. 15J). Angiotensin II also
stimulates the adrenal cortex to release
aldos-
terone,
which stimulates the kidneys to retain
sodium ions and water. The resulting increase
in blood volume contributes to increased blood
pressure. Normally, this mechanism ensures that
a decrease in blood flow to the kidneys is fol-
lowed by an increase in arterial pressure, which,
in turn, restores blood F
ow to the kidneys. If the
decreased blood F
ow is the result of disease, such
as atherosclerosis, the mechanism may cause
high blood pressure and promote further dete-
rioration of the arterial system.
In some individuals, high sodium intake
leads to vasoconstriction, raising blood pres-
sure. Obesity also is a risk factor for hyperten-
sion because it increases peripheral resistance.
Psychological stress, which activates sympathetic
nerve impulses that cause generalized vaso-
constriction, may also lead to hypertension. Yet
another cause of hypertension may be an inabil-
ity of endothelium to respond to a relaxing factor,
leading to vasoconstriction.
Hypertension is called a “silent killer”
because it may not have direct symptoms, yet
can raise the risk for serious cardiovascular com-
plications. ²or example, as the left ventricle works
harder to pump blood at a higher pressure, the
myocardium thickens, enlarging the heart. If the
coronary blood vessels cannot support this over-
growth, parts of the heart muscle die and ±
brous
tissue replaces them. Eventually, the enlarged
and weakened heart dies.
Hypertension also contributes to the devel-
opment of atherosclerosis. As arteries accumu-
late plaque, a
coronary
thrombosis
or a
coronary
embolism
may occur. Similar changes in the arter-
ies of the brain increase the chances of a
cerebral
vascular accident
(CVA), or stroke, due to a cere-
bral thrombosis, embolism, or hemorrhage.
When an embolus or hemorrhage causes
a stroke, paralysis and other functional losses
suddenly appear. A thrombus-caused stroke is
slower. It may begin with clumsiness, progress
to partial visual loss, then a³
ect speech. One arm
becomes paralyzed, then a day later, perhaps an
entire side of the body is a³
ected. Table 15A lists
risk factors for a stroke.
A
transient ischemic attack
(TIA, or “mini-
stroke”) is a temporary block in a small artery.
Symptoms include difficulty in speaking or
understanding speech; numbness or weakness
in the face, upper limb, lower limb, or one side;
dizziness; falling; an unsteady gait; blurred vision;
or blindness. These symptoms typically resolve
within twenty-four hours with no lasting e³
ects,
but may be a warning of an impending, more
serious stroke.
Treatment of hypertension varies and may
include exercising regularly, controlling weight,
reducing stress, and limiting the diet to low-
sodium foods. Drugs, such as diuretics and/or
inhibitors of sympathetic nerve activity, may
help control blood pressure. Diuretics increase
urinary excretion of sodium and water, reducing
the volume of body F
uids. Sympathetic inhibitors
block the synthesis of neurotransmitters, such as
norepinephrine, or block receptor sites of e³
ec-
tor cells. Table 15B describes how drugs that treat
hypertension work.
15.5
CLINICAL APPLICATION
Hypertension
Reduced blood flow to kidneys
Kidneys release renin
Renin leads to the production
of angiotensin II
Angiotensin II causes vasoconstriction
Blood pressure elevated
Blood flow to kidneys returns
toward normal
FIGURE 15J
Renin stimulates production
of angiotensin II, which elevates blood
pressure.
TABLE
15A
|
Risk Factors for Stroke
Alcohol consumption
Diabetes
Elevated serum cholesterol
²amily history of cardiovascular disease
Hypertension
Smoking
Transient ischemic attacks
TABLE
15B
|
Drugs to Treat
Hypertension
Type of Drug
Mechanism of Action
Angiotensin-
converting
enzyme
(ACE) inhibitors
Block formation of
angiotensin II, preventing
vasoconstriction
Beta blockers
Lower heart rate
Calcium channel
blockers
Dilate blood vessels by
keeping calcium ions out
of muscle cells in vessel
walls
Diuretics
Increase urine output,
lowering blood volume
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