ANGIOTENSIN-I CONVERTING-ENZYME ACTIVITY IN URANYL-NITRATE INDUCED ACUTE-RENAL-FAILURE IN RATS

Angiotensin I converting enzyme (ACE) was measured in urine, serum, an d tissues from rats with acute renal failure (ARF) induced by a single subcutaneous injection (15 mg/kg BW) of uranyl nitrate (UN). Urine wa s collected daily until day 5, when rats were sacrificed by decapitati on for the obtention of blood serum and tissues. Other groups of rats were sacrificed on days 1 and 2. These rats showed proteinuria and pol yuria. The damage to the kidney proximal tubule was shown by (a) histo logical analysis at light and electron microscopy levels on days 1, 2, and 5, (b) the increase in urinary excretion of dipeptidyl aminopepti dase IV and N-acetyl-beta-D-glucosaminidase on days 1-5, and (c) the l ow molecular weight proteinuria pattern on day 1. In addition, the his tological analysis at the ultrastructural level showed normal glomerul i appearance on days 1 and 2, but structural alterations on day 5. The se data suggest that the increased urinary excretion of enzymes and pr oteins is a consequence of the tubular injury on days 1 and 2, and of tubular and glomerular injury on day 5. ACE activity increased in urin e an days 1-5 and in serum on day 5. Tissue ACE activity increased in lung, small intestine, and adrenal glands; and remained unchanged in t estis, aorta, brain, kidney, heart, and liver Our data suggest that: ( a) the increase in serum ACE may be secondary to the changes in tissue ACE activity, and (b) the urine ACE increase may be due to the kidney proximal tubule damage. This work supports the contention that an inc rease in urine ACE may be an indicator of injury to the proximal tubul e.