Abstract
4-Androsten-3-one-17-spirolactone, an antagonist of aldosterone at the kidney tubule level, which possesses a very weak if any glucocorticoid potency, promoted the loss of edema and ascites in intact aminonucleoside nephrotic rats without affecting their increased rate of secretion of aldosterone. The data suggest that in aminonucleoside nephrosis the increased rate of secretion of aldosterone is one of the main factors operating in fluid retention.