Angiotensin II administration to rats during 6 weeks causes decreased activity of catalase and glutathione peroxidase in renal cortex. Rats show mild hypertension, subclinical signs of renal injury, increased glomerular expression of desmin, glomerular and interstitial expression of α-smooth muscle actin and an increased number of ED-1-positive cells in glomeruli. An inverse correlation exists between catalase activity and glomerular α-smooth muscle actin expression and between glutathione peroxidase activity and glomerular desmin expression. The decrease of antioxidant enzyme activity, early after angiotensin II administration, might be an important initiating factor in the complex process leading eventually to renal sclerosis by reduction of reactive oxygen intermediate breakdown. The significant relationship between markers of sclerosis and some antioxidant enzyme activities suggests either a causative link or a common triggering factor.