The regulation of sodium metabolism and the renin-angiotensin-aldosterone system was evaluated during 24 h of water, but not food, deprivation and during rehydration in the dog. Dehydration caused increases in plasma concentrations of sodium (6.0 +/- 0.7 meq/l), protein (0.8 +/- 0.1 g/dl), vasopressin (5.3 +/- 0.9 pg/ml), and renin activity (3.5 +/- 1.1 ng AI X ml-1 X 3 h-1). Plasma aldosterone was unchanged and plasma potassium fell slightly (0.2 +/- 0.1 meq/l). During dehydration, food, and thus sodium intake fell by more than 10% in 12 of 19 dogs, but urinary sodium excretion increased significantly, leading to a negative sodium balance (1.9 +/- 0.2 meq/kg). Sodium retention was observed after rehydration and sodium balance; plasma electrolytes, vasopressin, and plasma renin activity (PRA) returned turned to control levels after the 1st day of recovery. However, plasma aldosterone was slightly elevated at this time, returning to control after the 2nd day of recovery. The dehydration-induced natriuresis could not be accounted for by a fall in plasma aldosterone. However, sodium retention following rehydration could be aldosterone dependent, because additional studies showed a threefold rise in plasma levels of the hormone 1 h after drinking. The acute rise in aldosterone correlated closely (r = 0.82) with the fall in plasma sodium after drinking but not with changes in adrenocorticotrophic hormone, PRA, or plasma potassium. It is concluded that natriuresis is a homeostatic response to dehydration as a means of ameliorating the rise in body fluid osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)