Moreover, considering that the AT1R and AT2R blockers prevented the increase in systolic blood pressure promoted by TH in vivo, as well as the increase in cardiac TGF-β1 levels [19], it is plausible that the hemodynamic parameters altered in TH-induced cardiac hypertrophy may be influencing the elevated TGF-β1 levels in this model. This evidence concerns the gene AGTR1 and cardiac hypertrophy.