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Hypertension is the most common cardiovascular disease and a
precursor to other cardiovascular dysfunctions. The prevalence of
hypertension increases with age and varies based on race and coexisting
morbidities. Sustained arterial hypertension damages blood vessels
and such changes in the kidney, heart, and brain lead to an increased
incidence of renal failure, coronary disease, cardiac failure, and
stroke.
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The autonomic nervous system, especially the sympathetic branch,
plays a significant role in the regulation of blood pressure. A
general discussion of autonomic responses was presented in Chapter 4, specifically Table 4–3 and Figure 4–5. According
to the hydraulic equation, arterial blood pressure (BP) is directly
proportional to the product of the blood flow and the resistance
to passage of blood through the vessels. The estimate for blood
flow is cardiac output (CO), and the determinant for resistance
is peripheral vascular resistance (PVR). The hydraulic equation
is:
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In both normal and hypertensive individuals, blood pressure is
maintained by moment-to-moment regulation of cardiac output and
peripheral vascular resistance exerted at three anatomic sites (Figure
7–1). The primary locations are the precapillary arterioles,
postcapillary venules, and the heart. A fourth anatomic control
site, the kidney, contributes to maintenance of blood pressure by regulating
the volume of intravascular fluid volume, a slower, longer-lasting
control mechanism.
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Baroreflexes, mediated by autonomic nerves, act in combination
with humoral mechanisms, including the renal-mediated renin-angiotensin-aldosterone system,
to coordinate function at these four control sites and to maintain
normal blood pressure. Local release of vasoactive substances may
also be involved in the regulation of vascular resistance. For example,
nitric oxide (NO) and some prostaglandins dilate blood vessels. Other
local agents constrict vessels.
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Baroreflexes are responsible for rapid moment to moment adjustments
in blood pressure, such as in transition from a reclining to an
upright posture (Figure 7–2). Carotid baroreceptors are
stimulated by the stretch of the vessel walls brought about by the
internal blood pressure (Figure 7–2[1]).
Baroreceptor activation inhibits discharge (Figure 7–2[2])
of tonically active sympathetic neurons (Figure 7–2[3])
in the vasomotor center of the medulla. Conversely, reduction in
stretch results in a reduction in baroreceptor activity. Thus, in
the case of a transition to upright posture, baroreceptors sense
the reduced wall stretch that results from pooling of blood in the
veins below the level of the heart as reduction in arterial pressure,
and sympathetic discharge is increased. The increase in sympathetic
outflow acts through nerve endings to constrict the arterioles,
which increase peripheral vascular resistance. The sympathetic outflow
also increases cardiac output, both directly through stimulation
of the heart and through constriction of capacitance vessels that ...