Cardiac hypertrophy, characterized by an increase in cardiomyocyte size, enhanced fetal gene expression, accelerated interstitial cell proliferation, and a higher organization of the sarcomeric structure, is a compensatory mechanism in response to a variety of mechanical and neurohormonal stimuli such as Ang II, ET-1, catecholamines, and adrenaline [21, 22]. This evidence concerns the gene AGT and cardiac hypertrophy.