Persistent activation of the β-adrenergic and renin-angiotensin-aldosterone systems (RAS) is a hallmark of cardiac hypertrophy and subsequent heart failure, in which norepinephrine (NE) and angiotensin II (AngII) are the primary effectors that mediate the hypertrophic and fibrotic events in the heart [11–14]. This evidence concerns the gene AGT and cardiac hypertrophy.