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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.


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.

Figure 7–1.
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Anatomic sites of blood pressure control. These sites include vascular tone in venules and arterioles, the heart, and the kidney (by regulation of intravascular fluid volume).


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.


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 ...

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