Adjustment to aldosterone or desoxycorticosterone acetate induced sodium retention in patients with Addison's disease.

Long term administration of aldosterone (1) or desoxycorticosterone acetate (DCA) (2) to normal subjects has been shown, in certain instances, to produce continued renal potassium loss but only transient sodium and chloride retention. This adjustment of the renal response to sodium-retaining adrenal steroids has been termed an "escape" (3) from the expected effects of these compounds, and is seen clinically in the absence of edema with primary aldosteronism. The mechanism of this "escape" from sodium retention, that occurs despite continued excess of steroid sodium-retaining substances, is unknown. Some findings have suggested that the adrenal gland may play a role by producing a substance which either promotes sodium excretion or inhibits the sodium-retaining effect of other hormones. An adrenal cortical "salt-losing hormone" was postulated by Wilkins and Lewis (4) and Jailer (5) to explain renal salt loss in cases of congenital adrenal hyperplasia. Rosemberg (6) suggested that this might be explained by an aldosterone-inhibiting effect of certain 21-desoxypregnane steroids, and Klein and co-workers (7) reported that partially purified material from urine of patients with congenital adrenal hyperplasia caused increased urinary sodium excretion in rats. Recently, Neher, Meystre and Wettstein (8) reported the isolation of 3a,16a-dihydroxy-pregnan20-one from patients with the adrenogenital saltlosing syndrome and demonstrated a salt-losing potential of this steroid in adrenalectomized rats. Increased renal sodium excretion has been re-