Relationship of sodium retention to potassium excretion by the kidney during administration of desoxycorticosterone acetate to dogs.

T HE EFFECT of desoxycorticosterone acetate (DCA) on potassium (K) metabolism has been investigated extensively in man, dog and rat; the characteristic response consists of kaluresis, hypokalemia and metabolic alkalosis. Dependence of these alterations in electrolyte metabolism on an adequate intake of sodium (Na) was recognized by Seldin, Welt and Cort (I). They reported that patients fed a low salt diet showed no detectable disturbance in K metabolism during administration of 20 “g/day of DCA for I month. In the same study, rats received DCA on a low Na intake without detectable alterations in K excretion, muscle electrolyte composition or serum electrolytes. Relman and Schwartz (2, 3) also reported that patients injected with large amounts of DCA or compound F on a low Na intake failed to develop kaluresis. Heretofore, no evidence has been presented concerning the mechanism by which a low Na diet might limit K excretion during DCA administration. The present study was undertaken to determine the effect of severely reduced urinary Na excretion on K output by the kidney during injection of DCA in dogs on a substantial Na intake. Dogs with thoracic inferior vena cava constriction were employed since they characteristically retain almost all administered salt and accumulate ascites. For these studies adrenalectomized animals were observed during maintenance on large doses of DCA (4). F or comparison, data are included on the effect of DCA in normal dogs at different levels of Na intake.