The results of this study demonstrate that blockade of AT1 receptors with AT1 antagonists reduced the systolic BP significantly, caused an improvement in the myocardial antioxidant reserve (serum catalase and SOD enzyme activity), decreased oxidative stress and reduced the histopathological changes induced in the pressure-overload rat model of AABIH and cardiac hypertrophy. The gene discussed is SOD1; the disease is cardiac hypertrophy.