Long‐term exposure to elevated aldosterone levels or activation of the mineralocorticoid receptors results in cardiac, vascular, and renal tissue injury with mechanisms that are independent of blood pressure levels. This evidence has been obtained in experiments conducted in hypertensive animal models and clinical studies involving patients with heart failure, essential hypertension, and primary aldosteronism. Animal studies have indicated that aldosterone causes cardiovascular and renal tissue damage only in the context of an inappropriate salt status. It has been also suggested that some of the untoward effects of high‐salt intake might depend on activation of mineralocorticoid receptors resulting from increased generation of reactive oxygen species and changes in the intracellular redox potential. Although the interaction between dietary salt intake and circulating aldosterone in causing organ damage has received robust support from the results of animal experiments, the evidence of such interaction in the clinical setting is only preliminary and will require further investigation in appropriately designed studies. This article is protected by copyright. All rights reserved.