In another hypertrophy model induced by abdominal aorta coarctation, Huang et al. [58] revealed that exogenous administration of H2S significantly suppressed the development of cardiac hypertrophy and also greatly downregulated the Ang-II levels in cardiac tissue, suggesting that H2S plays a pivotal role in the development of pressure overload-induced cardiac hypertrophy. This evidence concerns the gene AGT and cardiac hypertrophy.