The secretion of aldosterone by the zona glomerulosa of the adrenal glands is of critical importance for the regulation of sodium and potassium balance. Aldosterone-deficient states are associated with negative salt balance and hyperkalemia, while the clinical syndromes due to aldosterone excess are associated with salt retention and hypokalemia. The overall role of aldosterone on sodium and potassium transport is regulated mainly through its effects on the kidney. In addition to its effect on renal tubular transport of sodium and potassium, aldosterone exerts an effect on hydrogen ion transport at the level of the collecting duct. At this site of the nephron, aldosterone enhances hydrogen ion secretion directly as well as indirectly through its effect on sodium transport. Studies using isolated tubules from mammalian kidneys indicate that the direct effect of this hormone on hydrogen ion transport is exerted at the level of the medullary portion of the collecting duct where it does not affect net sodium transport. At the cortical portion of the collecting duct, aldosterone increases sodium reabsorption and, in turn, promotes hydrogen ion and potassium secretion. In this article, we first briefly summarize the renal effects of aldosterone as a prelude to the following sections which are devoted to the pathophysiology and clinical manifestations of aldosterone deficiency or excess. Syndromes mimicking aldosterone deficiency or excess are also considered.
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