Aldosterone in Congestive Heart Failure

The potent mineralocorticoid aldosterone has a multifaceted role in the pathogenesis of congestive heart failure. In addition to its contribution to salt and water retention, it also promotes organ fibrosis. Although angiotensin-converting–enzyme inhibitors have important therapeutic benefit in heart failure, they do not eliminate the effects of aldosterone. Thus, recent studies have underscored the value of aldosterone-receptor antagonists, such as spironolactone, in the treatment of chronic heart failure. This review article gives an in-depth update on the mechanisms of action of aldosterone and their implications for therapy. Aldosterone was isolated from blood and urine, its adrenal origin elucidated, and its steroid structure identified nearly 50 years ago. Actions involving the reabsorption of sodium and the release of potassium by epithelial cells in the kidneys, intestine, and sweat and salivary glands led to its designation as a mineralocorticoid. The physiologic importance of aldosterone in preventing the loss of salt and water during periods of dietary sodium deprivation is now clear. Its contribution to the retention of sodium in patients with congestive heart failure, cirrhosis, and the nephrotic syndrome has also been established. 1 – 3 The perception of its pathophysiologic . . .