The activation of the MAPK signaling pathway plays an important role in cardiac hypertrophy [2], and the activation of mitogen-activated protein kinase p38 (p38-MAPK) is associated with multiple stimuli, such as angiotensin II (Ang II), endothelin 1 or catecholamine-induced cardiac hypertrophy and fibrosis [3], whereas the inhibition of p38-MAPK improves vascular function in the aorta and kidneys of Ang II-treated mice [4]. This evidence concerns the gene AGT and cardiac hypertrophy.