Although the exact pathogenetic mechanisms of the renal ischemia-reperfusion injury(I-R injury) have not been clearly elucidated yet, the reactive oxygen spe-cies(ROS) and mononuclear cell infiltration have been suggested to contribute to this renal injury process. The cytokines and growth factors produced by infiltrated leukocytes and renal parenchymal cells could accelerate the process of tissue damage by inducing cellular proliferation, fibrosis, and further recruitment of other inflammatory cells. The renin-angiotensin sys- tem(RAS) also has been suggested to be one of the most important mediators in the renal injury process of many animal models and human renal diseases. In order to evaluate the change of the levels of TNF-alpha, endothelin-l, and TGF-beta gene expression in unilateral I-R injured renal cortical tissue, competitive RT-PCR was performed for the above mRNAs in Sprague-Dawley rats(60 minutes of ischemic time by non-traumatic vessel clamp and 24 hours of reperfusion). Also the plasma renin activity(PRA) and an-giotensin II(AII) level were measured at the time of sacrifice by radioimmunoassay. On the light miscroscopic examination, I-R injured renal cortical tissue showed typical findings of acute tubular necrosis, such as mononuclear ceU infiltration, necrosis, swelling and denudation of proximal tubular cells. Compared to control sham operated group, I-R injured group tissues showed significantiy increased level of TGF-beta(p<0.05), endothelin-l(p<0.05) and TNF-alpha(p<0.05) gene expression in 24 hours after I-R renal injury. The levels of PRA and AIl were also significantly elevated compared to sham group(p< 0.05, p<0.05, respectively). In conclusion, we speculate that the early activation of RAS and elevated gene expression of TNF-alpha, endothelin and TGF-beta of renal cortieal tissue may contribute to the early pathogenetic mechanism of I-R renal injury process.