Although the formation of Ang II levels at the initial stages for a brief period activates redox-dependent sensitive mechanisms in the heart and contributes to adaptive cardiac hypertrophy, prolonged period of Ang II-induced increased disturbance in the pro-/antioxidants balance due to excess production of ROS in hypertrophied myocardium has shown markedly depressed cardiac function and progression of heart failure [23,61,96,97,98,99,100]. This evidence concerns the gene AGT and cardiac hypertrophy.