• Nina Queisser and Nicole Schupp.
• Institute of Pharmacology and Toxicology, University of Würzburg, Versbacher Str. 9, 97078 Würzburg, Germany.
• Free Radic. Biol. Med. 2012 Jul 15;53(2):314-27.

AbstractThe mineralocorticoid aldosterone regulates electrolyte and fluid balance and is involved in blood pressure homoeostasis. Classically, it binds to its intracellular mineralocorticoid receptor to induce expression of proteins influencing the reabsorption of sodium and water in the distal nephron. Aldosterone gained special attention when large clinical studies showed that blocking its receptor in patients with cardiovascular diseases reduced their mortality. These patients present increased plasma aldosterone levels. The exact mechanisms of the potential toxic effects of aldosterone leading to cardiovascular damage are not known yet. The observation of reduced nitric oxide bioavailability in hyperaldosteronism implied the generation of oxidative stress by aldosterone. Subsequent studies confirmed the increase of oxidative stress markers in patients with chronic heart failure and in animal models of hyperaldosteronism. The effects of reactive oxygen species have been related to the activation of transcription factors, such as NF-κB. This review summarizes the present-day knowledge of aldosterone-induced oxidative stress and NF-κB activation in humans and different experimental models.Copyright © 2012 Elsevier Inc. All rights reserved.

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