Toward a Broader Understanding of Aldosterone in Congestive Heart Failure


Discovered some 50 years ago, aldosterone (ALDO) has come to be recognized as a mineralocorticoid hormone with well-known endocrine properties in epithelial cells that contribute to the pathophysiology of congestive heart failure. This includes Na+ resorption at the expense of K+ excretion in classic target tissues: kidneys, colon, sweat and salivary glands. Though less well known, Mg2+ excretion is likewise enhanced by ALDO, while adrenal ALDO secretion is regulated by extracellular Mg2+ ([Mg2+]o). An emerging body of information has and continues to identify other endocrine actions of ALDO receptor-ligand binding. They include: promoting an efflux of cytosolic free Mg2+, or [Mg2+]i, in exchange for Na+ in such non-epithelial cells as peripheral blood mononuclear cells; its influence on endothelial cell function; and its central actions that involve regulation of cerebrospinal fluid composition produced by epithelial cells of the choroid plexus, activity of the hypothalamic paraventricular nucleus involved in Na+ appetite, Na+ and H2O excretion and sympathetic nerve activity, and the regulation of TNF-alpha production from central and/or peripheral sources. Extra-adrenal steroidogenesis and auto/paracrine properties of ALDO generated de novo in the cardiovasculature are now under investigation and preliminary findings suggest they contribute to tissue repair. The past decade has witnessed a revival of interest in this steroid molecule. In years to come, an even broader understanding of ALDOs contribution to the pathophysiology of congestive heart failure will undoubtedly emerge.

Authors: Karl T Weber, Yao Sun, Linus A Wodi, Ahmad Munir, Eiman Jahangir, Robert A Ahokas, Ivan C Gerling, Arnold E Postlethwaite, Kenneth J Warrington
Keywords: aldosterone, heart failure, renin-angiotensin system
DOI Number: 10.3317/jraas.2003.024      Publication Year: 2003

To search for other research papers by topic, keyword, author, or year, please go to our Publications page.