Published online before print July 18, 2005, doi: 10.1161/01.HYP.0000174329.99569.52
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(Hypertension. 2005;46:265.)
© 2005 American Heart Association, Inc.
Editorial Commentaries |
Cardiovascular Benefits of Aldosterone Receptor Antagonists
What About Potassium?
From the Harvard Medical School, and Brigham and Women’s Hospital, Boston, Mass.
Correspondence to Gordon H. Williams, Harvard Medical School, and Brigham and Women’s Hospital, 221 Longwood Ave, Boston, MA. E-mail gwilliams@partners.org
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Before the mid-1990s, much data supported the hypothesis that the primary mechanism action of aldosterone was to maintain sodium, volume, and potassium homeostasis. This is accomplished by a direct effect on epithelial cells of the distal segments of the nephron to actively promote sodium transport out of and potassium transport into the tubular lumen. This primary mechanism of action was reinforced by the 2 major mechanisms controlling adrenal aldosterone secretion: activation of the renin-angiotensin system (RAS) and, specifically, the concentration of angiotensin II, and the level of potassium.1
For nearly 50 years, inappropriate activation of the renin-angiotensin-aldosterone system (RAAS), with a particular emphasis on increased angiotensin II production, has been documented to be a risk factor for cardiovascular disease. Less well appreciated are the adverse effects of the other major outcome from activation of the RAAS: potassium reduction. In experimental animals and humans, potassium reduction increases cardiovascular risk, and potassium replacement reduces it. Because of the adverse effects of potassium reduction, inhibitors of the mineralocorticoid receptor have been used for many years to counteract the adverse effects of thiazide diuretics or an activated RAAS. Because of potential adverse side effects from spironolactone, the only mineralocorticoid receptor antagonist available at the time, other potassium-sparing diuretics were developed, among them triamterene.
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Nonepithelial Aldosterone-Induced Cardiovascular Injury |
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During the past 10 years, an increasing body of evidence has suggested that aldosterone and specifically activation of the mineralocorticoid receptor in nonepithelial cells also can induce cardiovascular damage. Data to support this conclusion come from clinical and experimental studies. The
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