The angiotensin I-converting enzyme (ACE) activity was measured in urine, serum, and tissues from rats with carbon tetrachloride (CCl4)-induced acute renal failure on days 1, 2, 3, and 7 after CCl4 administration. Serum ACE increased on days 1 to 3. Heart, lung, small intestine, brain, and testis ACE decreased, whereas kidney and liver ACE remained unchanged. Urine ACE activity increased from day 1 to day 3. Our data suggest that the increase in serum ACE may be secondary to the ACE release from the damaged tissues, and that the urine ACE increase may be due to the kidney proximal tubule damage. This work supports the contention that an increase in urine ACE may be an indicator of damage to the proximal tubule.