Abstract
Untreated adrenalectomized rats given 4 doses of water at hourly intervals showed a delayed diuresis and marked susceptibility to water intoxication. When treated with doses of desoxycorticosterone acetate (DCA), the response to water diuresis was directly proportional to the dose and, with 2.0 mg. or more, all symptoms of water intoxication disappeared. When rats were adrenalectomized 5 and 8 days and maintained on 1.0 mg. DCA/day, their response to water diuresis was no greater than for one-day-adrenalectomized controls, but they were protected against convulsions and death from water intoxication. Additional DCA prior to the adm. of water did not in any way alter this response. Adrenalectomized rats maintained on saline showed a delayed diuresis and a mortality similar to the one-day-adrenalectomized controls. Epinephrine HC1, when given to one-day-adrenalectomized rats, increased the diuresis from 21-64% and decreased the mortality from 72 to 0%. When 1.0 mg. DCA was given in combination with epinephrine, the excretion increased from 20-68%. With 3.0 mg. DCA plus epinephrine the excretion increased to 79%. Epinephrine HC1 given to 8-day adrenalectomized rats maintained on saline increased the excretion from 23-49%; while epinephrine given to DCA-maintained adrenalectomized rats increased the diuresis from 17-79%. Additional DCA in combination with the epinephrine did not further enhance this response. In all of these expts. there was definite protection from convulsion and death from water intoxication. The increased diuresis with epinephrine, and the protection of DCA against symptoms of water intoxication in face of delayed diuresis, may be explained by either an effect of epinephrine on the kidney or the effect of DCA on the distribution of water between extracellular and intracellular compartments and preventing excessive intracellular hydration.