Aldosterone is a kaliuretic hormone. It is also widely believed to be instrumental for physiological renal sodium sparing. How, then, can mammals respond to incipient dehydration or low sodium intake without inappropriate potassium loss? To study this problem angiotensin II (A II) was infused intravenously in six dogs. The dose rate was 10 ng per kg per min, probably maintaining plasma A II in the upper physiological range. The A II infusions lasted 3 h, i.e. long enough for the effects of increased aldosterone release to be observable. Mean arterial blood pressure increased by 8% while effective renal plasma flow and glomerular filtration rate fell by 28% and 7%, respectively. Renal sodium excretion fell to near 8% of the preinfusion control values. Plasma aldosterone increased three-fold. Yet no kaliuresis occurred. Potassium and chloride excretion declined by 50% and 80%, respectively. In five of the six dogs urine flow decreased 50% or more with concomitant increase of urine osmolality. Our data indicate that physiological increments of A II can bring about sustained renal sodium sparing without inducing potassium wasting.