The therapeutic response to pituitary adrenocorticotropic hormone is often accompanied by profound changes in water, solid, and electrolyte distribution. Metabolic balance studies in patients receiving corticotropin (1) have demonstrated marked initial retention of sodium and chloride and subsequently increased excretion of these ions while potassium balance remained negative. Bartter and his co-workers (2), studying patients with panhypopituitarism who were receiving corticotropin, observed that retention of sodium was greater than that of chloride, and concluded that sodium entered cells when corticotropin was given, and left the cells during the recovery periods. There was a large but transient loss of potassium within 24 hours after the beginning of treatment and a corresponding retention of potassium at the beginning of the postcorticotropin period. A transient increase in the inulin space in patients treated with corticotropin and cortisone, and maintained on rigid salt restriction, has been reported by Levitt and Bader (3). Since the patients studied by these authors were on a markedly restricted salt intake and remained in salt balance, without gain in weight, it was concluded that the observed increase in the extracellular fluid volume was due to a shift of salt and water from the intracellular compartment. Recently, Ziff, Simson, and Bunim (4) reported variation in the manner of water re-