Discovered some 50 years ago, aldosterone (ALDO) has come to be recognised 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-α production from central and/or peripheral sources. Extra-adrenal steroidogenesi 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 ALDO's contribution to the pathophysiology of congestive heart failure will undoubtedly emerge.

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Toward a broader understanding of aldosterone in congestive heart failure