after a day to two despite continued infusion
of the vasoconstrictor. Therefore, with normal
renal function, an acute elevation in arterial
pressure caused by increasing systemic vascu-
lar resistance (or by stimulating the heart) is
compensated by a reduction in blood volume,
which restores the arterial pressure to normal.
Considerable evidence shows that in chronic
curve is shifted to the right so that a higher arte-
rial pressure is required to maintain sodium bal-
ance. The elevated pressure is sustained by an
increase in blood volume. These changes in renal
handling of sodium and water can be brought
about by changes in sympathetic activity and
hormones that affect renal function (e.g., angio-
tensin II, aldosterone, vasopressin). In addition,
altered kidney filtration and sodium balance
in renal disease can shift the pressure natriure-
sis curve to the right, leading to an increase in
blood volume and sustained hypertension.
Essential (Primary) Hypertension
Essential (or primary) hypertension accounts
for approximately 90% to 95% of patients
Essential hypertension
(90% -95% )
• U nknow n causes
• Involves:
- increased b lo o d volum e
- i ncreased system ic vascular resistance
(vascular disease)
• A ssociated w ith:
- heredity
- abnorm al response to stress
- diabetes and obesity
- age, race, and socioeconom ic status
Secondary hypertension
(5% -10% )
• Renal a rtery stenosis
• Renal disease
• H yperaldosteronism (p rim a ry )
• P heochrom ocytom a (catecholam ine-
secreting tu m o r)
• A o rtic coa rcta tion
• P regnancy (preeclam psia)
• H y p e rth yro id ism /h yp o th y ro id is m
• C ushing syndrom e (excessive g lu c o c o rti-
coid secretion)
• Sleep apnea
diagnosed with
This diagnosis is made after known causes of
hypertension (i.e., secondary hypertension)
are eliminated.
Therefore, essential hyper-
tension is a diagnosis by exclusion. Despite
many years of research, no unifying hypoth-
esis accounts for the pathogenesis of essential
hypertension. However, a natural progression
of this disease suggests that early elevations in
blood volume and cardiac output might pre-
cede and then initiate subsequent increases
in systemic vascular resistance. This has led
some investigators to suggest that the basic
underlying defect in hypertensive patients is
an inability of the kidneys to adequately han-
dle sodium. Increased sodium retention could
account for the increase in blood volume.
Indeed, many excellent experimental studies
as well as clinical observations have shown
that impaired renal natriuresis (sodium excre-
tion) can lead to chronic hypertension.
Besides the renal involvement in hyperten-
sion, it is well known that vascular changes can
contribute to hypertensive states, especially in
the presence of impaired renal function. For
associated with increased systemic vascular
resistance caused by a thickening of the walls of
resistance vessels and by a reduction in lumen
diameters. In some forms of hypertension, this
is mediated by enhanced sympathetic activity
or by increased circulating levels of angiotensin
II, causing smooth muscle contraction and vas-
cular hypertrophy Experimental studies have
suggested that changes in vascular endothelial
function may cause these vascular changes.
For example, in hypertensive patients, the vas-
cular endothelium produces less nitric oxide.
Nitric oxide, besides being a powerful vasodi-
lator, inhibits vascular hypertrophy. Increased
endothelin-1 production may enhance vascu-
lar tone and induce hypertrophy. Evidence sug-
gests that hyperinsulinemia and hyperglycemia
in type 2 diabetes (non-insulin-dependent dia-
betes) cause endothelial dysfunction through
increased formation of reactive oxygen species
and decreased nitric oxide bioavailability, both
of which may contribute to the abnormal vas-
cular function and hypertension often associ-
ated with diabetes.
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