This study used 16 hr/day measurement of renal blood flow (RBF) and arterial pressure (AP) to determine the role of nitric oxide (NO) in mediating the renal vasodilation caused by onset of Type I diabetes. The AP and RBF power spectra were used to determine the autoregulatory efficiency of the renal vasculature. Rats were instrumented with artery and vein catheters and a Transonic flow probe on the left renal artery, and were divided randomly into four groups: Control (C), Diabetes (D), Control plus L-NAME (CL), and Diabetes plus L-NAME (DL). Mean AP averaged 90±1 and 121±1 mmHg in the D and DL groups, respectively, during the control period, and RBF averaged respective 5.9±1.2 and 5.7±0.7 ml/min. Respective C and CL groups were not different. Onset of diabetes (STZ, 40 mg/kg, iv.) in D rats increased RBF gradually, but it averaged 55% above control by day 14. In the DL rats, on the other hand, RBF remained essentially constant, tracking with RBF in the non-diabetic C and CL control groups for the 2-week period. Diabetes did not change mean AP in any group. Transfer function (TF) analysis revealed impaired dynamic autoregulation of RBF overall, including the frequency range of tubuloglomerular feedback (TGF), and L-NAME completely prevented those changes as well. These data strongly support a role for NO in causing renal vasodilation in diabetes, and suggest that an effect of NO to blunt RBF autoregulation may play an important role.