One of the mechanisms by which Ang-(1-7) plays its effects in the heart is stimulating the nitric oxide (NO) production. Indeed, it has been demonstrated that Ang-(1-7) via Mas increases the synthesis of NO through a mechanism involving the activation of the endothelial NO synthase (eNOS). These effects were abolished by A-779 and are absent in cardiomyocytes from Mas-deficient mice [76] . Recently, Gomes et al. [77] found that the treatment of isolated cardiomyocytes of rats with Ang-(1-7) efficiently prevents the Ang-II-induced hypertrophy by modulating the calcineurin/NFAT signaling cascade. These effects were blocked by NO synthase inhibition and by guanylyl cyclase inhibitors, indicating that these effects are mediated by the NO/cGMP pathway.