Hypertension caused by elevated levels of the blood pressure-regulating hormone angiotensin II (AngII) leads to oxidative stress and DNA damage in kidneys of mice. In vitro-studies showed a role of the free radical-generating NADPH oxidase (Nox) in this damage. Here, we studied the contribution of the isoforms Nox1, 2 and 4 to AngII-induced oxidative stress and DNA lesions in the kidney. Male wildtype (WT) C57BL/6, Nox1-, Nox2- and Nox4-knockout (KO) mice were infused with either vehicle or AngII during 28 days. Afterwards, urine and kidneys were analyzed for markers of oxidative stress and DNA damage. In WT mice, AngII induced hypertension, elevated urinary albumin levels and formation of ROS and DNA damage in the kidney. In Nox2- and Nox4-KO mice blood pressure was as high as in WT mice but lower in Nox1-KO mice. A rise in urinary albumin and systemic oxidative stress due to AngII was observed in all KO mice. In kidney tissue, only Nox1-KO mice showed no significant ROS formation. Basal values of genomic damage were higher in Nox2- and Nox4-KO mice. Only in Nox1-KO mice AngII did not cause significantly more DNA double strand breaks than in the controls. Nox1 seems to be mostly responsible for the AngII-induced generation of ROS in mouse kidney. Surprisingly, genomic damage in kidneys of Nox2- and Nox4-KO mice was already increased in the absence of AngII.