The effect of val-äangiotensin-II-amide on tubular sodium and water reabsorption in the rat kidney was studied by micropuncture techniques. An angiotensin infusion of 0.2–0.5 µg/min/kg caused a significant increase ( + 16 mEq/l) in the sodium concentration of tubular fluid collected from the distal tubule, as compared to collections made from the same site of the tubule during saline infusion alone. TF/P-inulin ratio remained unchanged. Glomerular filtration rate, sodium and water excretion were unaltered. During an angiotensin infusion of 1.0-1.5 µg/min/kg a similar elevation of the distal tubular sodium concentration was observed, but TF/P-inulin ratio decreased significantly. Urinary water and sodium excretion increased. An elevation of the intratubular concentration of angiotensin to 2.5 µg/ml had no effect upon tubular reabsorptive capacity, as measured by the ‘split oil-droplet method’ in the proximal or in the distal tubule. Direct application of angiotensin from the capillary side of the tubule by peritubular perfusion did not alter ‘reabsorptive half-time’ in the proximal tubule, but caused a significant prolongation of ‘reabsorptive half-time’ in the distal tubule from 35.6–67.7 sec. These results demonstrate that angiotensin, offered from the capillary side of the tubule, directly inhibits sodium reabsorption in the distal tubule.