Recently, in MI rats randomized to receive either vehicle, the ACEI enalapril, or the ARB candesartan for 8 weeks, Ocaranza et al. [52] observed that both drugs prevented LVH and increased plasma Ang-(1-9) levels by several folds. Ang-(1-9) levels correlated negatively with different LVH markers with or without adjustment for BP reduction. This effect was specific as neither Ang-(1-7), Ang II nor bradykinins were correlated with LVH. Chronic administration of Ang-(1-9) to MI rats by osmotic minipumps versus vehicle for two weeks decreased plasma Ang II levels, inhibited ACE activity and also prevented cardiac myocyte hypertrophy. Because there are in vitro evidences that the incubation of Ang-(1-9) with ACE generates Ang-(1-7) [9] , and Ang-(1-7) negatively regulates hypertrophy [34, 117] , the authors used the Ang-(1-7) receptor blocker A779 to investigate whether Ang-(1-7) could mediate the effects of Ang-(1-9). Even though A779 was bioactive, with significant increase in circulating Ang-(1-7) levels by 2.7 fold, this compound did not modify the Ang-(1-9)-dependent suppression of cardiac myocytes hypertrophy induced by MI [52] . In in vitro experiments with cardiac myocytes incubated with norepinephrine (10 μM) or with IGF-1 (10 nM), Ang-(1-9) also prevented hypertrophy and this effect was not modified by the coincubation with Ang-(1-9) and A779 [52] .