Peripheral Autoregulatory Components

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These baroreceptor reflex mechanisms may be blunted in the elderly

and in those with diabetes.


Stimulation of certain areas within the central nervous system
(e.g., nucleus tractus solitarius, vagal nuclei, vasomotor center, and
the area postrema) can either increase or decrease BP. For example,
2-adrenergic stimulation within the central nervous system decreases
BP through an inhibitory effect on the vasomotor center.However, angiotensin
II increases sympathetic outflow from the vasomotor center,
which increases BP.
The purpose of these neuronal mechanisms is to regulate BP and
maintain homeostasis. Pathologic disturbances in any of the four major
components (autonomic nerve fibers, adrenergic receptors, baroreceptors,
or central nervous system) conceivably could lead to chronically
elevated BP. These systems are physiologically interrelated. A
defect in one component may alter normal function in another, and
such cumulative abnormalities then may explain the development of
essential hypertension.

PERIPHERAL AUTOREGULATORY COMPONENTS

Abnormalities in renal or tissue autoregulatory systems could cause


hypertension. It is possible that a renal defect in sodium excretion may
develop first, which can then cause resetting of tissue autoregulatory
processes, resulting in a higher arterial BP.
The kidney usually maintains normal BP through a volumepressure
adaptive mechanism. When BP drops, the kidneys respond
by increasing retention of sodium and water. These changes lead to
plasma volume expansion, which increases BP. Conversely, when BP
rises above normal, renal sodium and water excretion are increased
to reduce plasma volume and cardiac output. This ultimately will
maintain homeostatic BP conditions.
Local autoregulatory processes maintain adequate tissue oxygenation.
When tissue oxygen demand is normal to low, the local
arteriolar bed remains relatively vasoconstricted. However, increases
in metabolic demand trigger arteriolar vasodilation that lowers peripheral
vascular resistance and increases blood flow and oxygen delivery
through autoregulation.
Intrinsic defects in these renal adaptive mechanisms could lead
to plasma volume expansion and increased blood flow to peripheral
tissues, even when BP is normal. Local tissue autoregulatory
processes that vasoconstrict then would be activated to offset
the increased blood flow. This effect would result in increased
peripheral vascular resistance and, if sustained, also would result
in thickening of the arteriolar walls. This pathophysiologic component
is plausible because increased total peripheral vascular resistance
is a common underlying finding in patients with essential
hypertension.

VASCULAR ENDOTHELIAL MECHANISMS

Vascular endothelium and smooth muscle play important roles in regulating


blood vessel tone and BP. These regulating functions are mediated
through vasoactive substances that are synthesized by endothelial
cells. It has been postulated that a deficiency in the local synthesis of
vasodilating substances (e.g., prostacyclin and bradykinin) or excess
vasoconstricting substances (e.g., angiotensin II and endothelin I)
contribute to essential hypertension, atherosclerosis, and other
diseases.
Nitric oxide is produced in the endothelium, relaxes the vascular
epithelium, and is a very potent vasodilator. The nitric oxide system is
an important regulator of arterial BP. Hypertensive patients may have
an intrinsic deficiency in nitric oxide release, resulting in inadequate
vasodilation. Although the exact role of nitric oxide in hypertension
is unclear, it may be a pharmacologic target in the future.

ELECTROLYTES AND OTHER CHEMICALS

Epidemiologic and clinical data have associated excess sodium intake


with hypertension. Population-based studies indicate that high-salt diets
are associated with a high prevalence of stroke and hypertension.
Conversely, low-salt diets are associated with a low prevalence of
hypertension. Clinical studies have shown consistently that dietary
sodium restriction lowers BP in many (but not all) patients with elevated
BP. The exact mechanisms by which excess sodium leads to
hypertension are not known. However, they may be linked to increased
circulating natriuretic hormone, which would inhibit intracellular
sodium transport, causing increased vascular reactivity and
increased BP.
Altered calcium homeostasis also may play an important role in
the pathogenesis of hypertension. A lack of dietary calcium hypothetically
can disturb the balance between intracellular and extracellular
calcium, resulting in an increased intracellular calcium concentration.
This imbalance can alter vascular smooth muscle function by
increasing peripheral vascular resistance. Some studies have shown
that dietary calcium supplementation results in a modest BP reduction
in hypertensive patients.
The role of potassium fluctuations is also inadequately understood.
Potassium depletion may increase peripheral vascular resistance,
but the clinical significance of small serum potassium concentration
changes is unclear. Furthermore, data demonstrating reduced
cardiovascular risk with dietary potassium supplementation are very
limited. This issue requires further investigation before potassium
supplementation can be endorsed.
Hyperuricemia has been associated with an increased risk of cardiovascular
events in hypertensive patients but remains controversial
because of inconsistent data. Uric acid has no physiologic function
and is considered a biologicwaste product. Therefore, there is no rational
explanation describing why uric acid would cause cardiovascular
harm. However, elevated uric acid may be viewed

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