Background Shortly after the structure of aldosterone (aldo) was determined (1) in 1952, its effect on the kidney to cause sodium (Na) retention and potassium (K) and hydrogen ion (H) excretion were characterized (2,3). Although the ability of aldo to effect many transporting epithelia is now well known, it is this effect on the kidney to retain sodium which is felt to play an important role in Na retention to cause edema and, in some settings, hypertension (HBP).