Angiotensin II(ANG II) plays an important role in the regulation of systemic and renal hemodynamics, and functions as a growth factor in various tissues. ANG II is also known to be associated with healing after tissue injuries as profibrotic molecule. To determine effects of ANG II itself on kidney and to know its mechanism of action, 36 adult male Sprague-Dawley rats were infused with ANG II at a dose of 50ng/min(low ANG group), 100ng/min(high ANG group), or vehicle(control group) for 1 week using osmotic minipump(Model 2001D, Alza Co, USA) inserted into the interscapular area of the back. Tissue fibrosis was quantitated morphometrically using point detection method after Masson-Trichrome stain. Expression of ED-1 was determined by immunohistochemical staining. Immunohistochemical stain, RT- PCR, and Western blot assay were done for TGFbeta1 mRNA and protien. Results were as follows:1) There were no differences in body weight or kidney weight/body weight among 3 groups. 2) Interstitial volume was increased significantly in the low and high ANG groups compared with the control group(P<0.05) 3) ED-1 positive cells were increased significantly in the the low and high ANG groups compared with the control group(P<0.05). 4) TGFbeta1 mRNA and protein expression were increased significantly in the low and high ANG groups compared with the control group(P<0.05). Therefore, regardless of systemic hypertension, ANG II infusion induced renal fibrosis and increased expression of TGFbeta1 mRNA and protein in the kidney of the Sprague-Dawley rat.