Increased activity of the renin angiotensin aldosterone system (RAS) leads to hypertension and oxidative stress. A stimulated RAS can also cause an inappropriate increase of the mineralocorticoid hormone aldosterone (Ald), predominantly in a subgroup of hypertensive patients. Epidemiological studies revealed a higher cancer mortality and an increased kidney cancer incidence in hypertensive patients. Among other factors, elevated concentrations of angiotensin II (AngII) or Ald, or the combination of both might contribute to carcinogenesis, in particular of the kidney. Experimental hypertension models were used to analyse the effect of increased blood pressure and of increased levels of AngII and Ald on the genomic integrity of kidney cells. Mice equipped with osmotic mini pumps, delivering AngII in four different concentrations between 60 ng/kg min and 1 mg/kg min during 28 days revealed a dose-dependent increase of superoxide radical production in kidney tissue, as well as a dose-dependent increase of double strand breaks, detected by an antibody against g-H2AX. In kidneys of the DOCA/salt rat, which develops a mineralocorticoid-dependent hypertension, additionally a higher amount of the potentially mutagenic base modification 7,8-dihydro-8-oxo-guanine was detected. Rats equipped with osmotic mini pumps delivering Ald served to answer the question if the DNA damage is caused by the hypertension or by the elevated Ald concentration. Therefore they were additionally treated with the mineralocorticoid receptor blocker spironolactone, the antioxidant tempol and the vasodilator hydralazin. Results from this experiment as well as from the DOCA/salt rats suggest the increased hormones to be the cause of damages.