1. In the United States, the prevalence of hypertension is higher among African Americans
than among non-Hispanic whites or Mexican Americans. The data are from the Third
National Health and Nutrition Examination Survey (NHANES III).

2. Slide 1
Sequelae of Essential Hypertension
• Uncontrolled hypertension is associated with such complications as heart
failure, myocardial infarction and stable or unstable angina pectoris,
stroke, renal failure, and retinopathy1
• Increased tension on the arterial wall accounts for hemorrhagic stroke,
aortic dissection, and acute pulmonary edema2
• High blood pressure contributes to atherogenesis and acute
cardiovascular events through increased sympathetic activity and
stimulation of the renin-angiotensin-aldosterone system2
• Pathogenetic mechanisms present in hypertension combine to produce
endothelial dysfunction, which occurs in diabetes mellitus and dyslipidemia
as well as hypertension2

3. Slide 9
Aldosterone: Important Component of
Renin-Angiotensin-Aldosterone System
• The physiologic function of the renin-angiotensin-aldosterone system (RAAS) is to maintain volume and electrolyte
homeostasis and to set blood pressure1
• Besides acting directly on the kidneys, the RAAS modulates activity of the heart and blood vessels to ensure adequate
tissue perfusion2
• Angiotensin II (Ang II), the most active effector substance of the RAAS, is formed in a cascade triggered by the release
of renin from the kidneys; Ang II in turn stimulates the adrenal cortex to secrete the mineralocorticoid aldosterone1
• Chronic elevation of Ang II and/or aldosterone has pathophysiologic effects on the cardiovascular system1
• Although angiotensin-converting enzyme inhibitors limit Ang II synthesis and Ang II blockers compete with Ang II for its
AT1
receptors, pharmacologic doses of these agents do not completely suppress the RAAS, particularly aldosterone1
• Moreover, aldosterone synthesis, which causes the kidneys to retain sodium and water at the expense of potassium and
magnesium loss, can occur independently of Ang II stimulation1,3
1. Mortensen RM, Williams GH. Aldosterone action. In: DeGroot LJ, Jameson JL, eds. Endocrinology. 4th ed.
Philadelphia, Pa: WB Saunders; 2001:1783-1789.
2. Rocha R, Stier CT, Jr. Pathophysiological effects of aldosterone in cardiovascular tissues. Trends Endocrinol Metab.
2001;12:308-314.
3. Schafer JA. Renal water and ion transport systems. Adv in Physiol Educ. 1998;20:S119-S131.

4. Slide 10
Stimulators of Aldosterone
• Stimuli related to the renin-angiotensin-aldosterone system (RAAS)
include angiotensin II, while non-RAAS stimuli include elevated potassium
in extracellular fluid, adrenocorticotropic hormone (ACTH, corticotropin),
norepinephrine, endothelin, and serotonin1,2
• In contrast to the other compounds, nitric oxide is a negative modulator of
aldosterone3
1. Weber KT. Mechanisms of disease: aldosterone in congestive heart
failure. N Engl J Med. 2001;345:1689-1697.
2. Mortensen RM, Williams GH. Aldosterone action. In: DeGroot LJ,
Jameson JL, eds. Endocrinology. 4th ed. Philadelphia, Pa: WB Saunders;