In man and dogs, natriuresis is produced by angiotensin in some states associated with hyperaldosteronism more readily than in the normal state. In the rat, aldosterone has been reported to augment renin induced natriuresis. To investigate these unexpected findings, 0.100 µg/kg/min of angiotensin was administered to normal, aldosterone treated and salt-depleted dogs. Natriuresis occurred in some normal dogs, but in none of the others. It was concluded that aldosterone does not augment and may inhibit natriuresis induced in dogs by angiotensin. Other aspects of renal function were also studied. Angiotensin was found less likely to induce natriuresis during a water diuresis than during an osmotic diuresis. The pressor response to angiotensin was significantly reduced by salt-depletion, but was not affected by aldosterone infusion. A salt load slightly increased the pressor response to angiotensin. In a comparative study, the pressor response to norepinephrine was found to be unaffected by salt-depletion. Data from 92 experiments confirmed the reported inverse correlation between mean control blood pressure and the pressor response to angiotensin. A similar, although much weaker, correlation existed for the pressor response to norepinephrine. Possible explanations for this phenomenon are discussed and the influence on it of variations in salt intake described.