Abnormal renal hemodynamic response to reduced renal perfusion pressure in diabetic rats: role of NO

Enhanced activity of endgenous NO in a diabetic rat model is likely to cause basal hyperfiltration and continuous renal vasodilation expressed at decreased renal perfusion pressures. Renal hemodynamic abnormalities detected in experimental diabetes are due to the abnormal activity of NO. The abnormal response curve of renal blood flow is not influenced by prostaglandin synthesis restriction with indomethacin.