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The investigation reported in this paper is concerned with the effects of desoxycorticosterone acetate (DCA), hydrocortisone and dietary potassium depletion on the elaboration of an osmotically concentrated urine in the hydropenic state. Loeb and his associates (1, 2) demonstrated that dogs maintained on large amounts of DCA develop a diabetes insipidus-like picture. Since then, renal function studies in man (3-5), dogs (6) and rats (7, 8) have shown that the ability of the kidney to concentrate the urine is markedly reduced in states of adrenal hyperfunction and potassium deficiency. The mechanism by which polyuria is produced under these conditions has not been established. In particular, the role of potassium deficiency is still a matter of controversy. Thus, contrary to Loeb and co-workers (1, 2), who were unable to prevent the development of polyuria in their DCA-treated animals by feeding potassium chloride, some authors maintain (9) that the increased loss of potassium following the administration of adrenal steroids is responsible for the impairment of water conservation. Also, there is no agreement on the sensitivity of the kidney to vasopressin (Pitressin®) during various states of potassium depletion (7, 9). The present study is an attempt to clarify some of these points. We have, in particular, studied the formation of a concentrated urine during osmotic diuresis in the hydropenic state. According to current concepts, an osmotically concentrated urine can be visualized as being made up of an isosmotic portion less the amount of water abstracted from it to produce hypertonicity ( 10, 11 ).

THE EFFECTS OF ADRENAL STEROIDS AND POTASSIUM DEPLETION ON THE ELABORATION OF AN OSMOTICALLY CONCENTRATED URINE*