Emerging evidence suggests that renal oxidative stress and nitric oxide (NO) deficiency is linked to cardiovascular disease and diabetic complications. Mechanisms are not clear, but exaggerated NADPH oxidase- and mitochondria-derived superoxide production and NO deficiency may impair vascular function and lead to impairment of renal autoregulation. Using a translational design, our projects aim to characterize the mechanisms for superoxide and NO formation, interaction and influence on renal, cardiovascular and metabolic functions in health and disease. Novel dietary and pharmacological therapeutic strategies, focusing on dampening of vascular oxidative stress, are investigated and characterized in experimental disease models and in patients with reno-cardio-metabolic disorders, including chronic kidney disease, hypertension and type 2 diabetes.