OBSERVATIONS ON THE POLYURIA PRODUCED BY DESOXYCORTICOSTERONE ACETATE

Abstract

In the dog with diabetes insipidus (d.i.), inj. of 2.5 mg. to 10 mg. daily of desoxycorticosterone acetate (DCA) markedly increased the severity of the d.i. Similar injs. in a normal dog resulted in a syndrome resembling very mild d.i. Pitressin only partially controlled DCA polyuria, even if given in dosage several times that required to render a dog with d.i. non-polyuric. During adm. of DCA, reduction of protein intake reduces the polyuria, but the change in urine vol. was less marked than when a similar expt. was performed on an ordinary d.i. dog. Increased N intake markedly increased DCA polyuria. Creatinine clearance studies showed that, both in normal and in d.i. dogs, DCA reduced tubular reabsorption of water. Dosages as large as 10 mg. daily also increased glomerular filtration, but smaller doses had little effect. In contrast to the results on dogs, DCA up to 30 mg. daily failed to increase the water exchange of normal cats. In cats with d.i., such injs. increased neither the severity of the d.i., nor the dosage of Pitressin required to relieve it. There is a discussion of the relation of these findings to the hypothesis that the adrenocortical hormone and the posterior lobe antidiuretic hormone are physiological antagonists.