ABSTRACT
Aldosterone is the primary endogenous mineralocorticoid steroid. It is synthesized within the adrenal zona glomerulosa from cholesterol, the last step being the sequential 11β-hydroxylation of deoxycorticosterone by the enzyme aldosterone synthase to yield corticosterone, 18-hydroxylation to yield 18-hydroxycorticosterone followed by another hydroxylation leading to the formation of a diol which then spontaneously dehydrates to form aldosterone. The synthesis of aldosterone is primarily regulated by angiotensin II (Ang II) and potassium, and to a lesser extent by ACTH (adrenocorticotropic hormone) and sodium. Aldosterone acts through mineralocorticoid receptors (MRs) in transport epithelium, primarily that of the renal tubules, colon and salivary glands, to promote sodium and water reabsorption and potassium and proton excretion. Hyperaldosteronism results in hypertension, suppression of the renin-angiotensin system (RAS), hypokalemia, and metabolic alkalosis. In addition to modulating the vectorial transport of ions and water, aldosterone acts upon non-epithelial tissues, notably the cardiovascular and central nervous systems, where it has trophic effects in addition to altering ion transport and compartmentalization.1-3
Because of the pathological cardiac, renal, and vascular remodeling associated with mineralocorticoid excess, it is crucial that conditions of excessive production of aldosterone be diagnosed and treated appropriately.
