While we were not able to find a significant increase in oxidative stress measured directly on kidney tissue neither with a redox-sensitive dye nor with an antibody against the oxidative base modification 8-oxodG or in urine in contrast to our previous studies with aldosterone- or angiotensin II-induced hypertension [20,28,29], we did find significantly increased excretion of the lipid peroxidation marker 15-isoprostane F2t. The gene discussed is AGT; the disease is Hypertension.