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From: Chapter
Chapter 3.
3. Hypertension
Hypertension

Pharmacotherapy: A Pathophysiologic Approach, 9e, 2014


Pharmacotherapy: A Pathophysiologic Approach, 9e, 2014

Legend:
Diagram representing the reninangiotensinaldosterone system. The interrelationship between the kidney, angiotensin II, and regulation of blood pressure is depicted.
Renin secretion from the juxtaglomerular cells in the afferent arterioles is regulated by three major factors to trigger conversion of angiotensinogen to angiotensin 1. The
primary sites of action for major antihypertensive agents are included: ACE inhibitors; angiotensin II receptor blockers; -blockers; calcium channel blockers;
diuretics; aldosterone antagonists; direct renin inhibitor.

Table 3-2 Potential Mechanisms of Pathogenesis


Blood pressure (BP) is the mathematical product of cardiac output and peripheral resistance. Elevated BP
can result from increased cardiac output and/or increased total peripheral resistance.
Increased cardiac output

Increased cardiac preload:


Increased fluid volume from excess sodium
intake or renal sodium retention (from reduced
number of nephrons or decreased glomerular
filtration)
Venous constriction:
Excess stimulation of the reninangiotensin
aldosterone system (RAAS)
Sympathetic nervous system overactivity

Increased peripheral resistance

Functional vascular constriction:


Excess stimulation of the RAAS
Sympathetic nervous system overactivity
Genetic alterations of cell membranes
Endothelial-derived factors
Structural vascular hypertrophy:
Excess stimulation of the RAAS
Sympathetic nervous system overactivity
Genetic alterations of cell membranes
Endothelial-derived factors

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