Background: Several reports suggest that increased generation or activity of nitric oxide (NO) have been implicated in the pathogenesis of glomerular hyperfiltration and hyperperfusion that occurs in early diabetes. However, the precise role of altered NO generation in the pathogenesis of diabetic nephropathy is unclear. The present study was aimed to investigate the role of NO in the pathogenesis of glomerular hyperfiltration and hyperperfusion in streptozotocin (STZ)-induced diabetic rats. Materials and Methods: The renal hemodynamic and renal function parameters, such as glomerular filtration rate (GFR), renal blood flow (RBF), and creatinine clearance, protein, sodium and potassium levels were determined. The above mentioned parameters were measured before and after administration of a nonspecific NO synthesis inhibitor, nitro-L-arginine methyl ester (L-NAME), in diabetic and control rats. Plasma NO and malondialdehyde (MDA), the last product of lipid breakdown caused by oxidative stress, levels were also measured. Results: Diabetic rats exhibited significantly elevated plasma NO levels, approximately two-fold higher than controls (p<0.001). L-NAME treatment prevented an increase in plasma NO concentrations in diabetic rats. GFR, RBF, and creatinine, protein, sodium and potassium excretions were significantly elevated in the diabetic animals. Inhibition of NO synthesis by L-NAME attenuated the RBF and GFR in diabetic rats but had no effect on the other parameters. L-NAME treated diabetic rats had a marked decrease in plasma MDA levels compared to the diabetes mellitus and control group. Conclusion: Renal hyperfiltration and hyperperfusion in diabetic rats increased in correlation with raised plasma NO levels. When NO is blocked, renal hyperfiltration and hyperperfusion in diabetic rats decreased. This suggests that the increase of NO levels might not be a single factor that is responsible for the changes in the pathogenesis in early diabetes.