To further understand the role of Ang-(1-9) compared to Ang-(1-7) in cardiomyocyte hypertrophy, Flores-Muñoz et al. [56] studied Ang-(1-9) effects in rat neonatal H9c2 and in rabbit left ventricular cardiomyocytes. Cardiomyocyte hypertrophy was stimulated with Ang II or vasopressin, significantly increasing cell size by approximately 1.2-fold as well as stimulating expression of the hypertrophy gene markers atrial natriuretic peptide, brain natriuretic peptide, β-myosin heavy chain and myosin light chain (2-to 5fold). Both Ang-(1-9) and Ang-(1-7) were able to block hypertrophy induced by either agonist. The effects of Ang-1-9) were not inhibited by captopril, supporting previous evidence that Ang-(1-9) acts independently of Ang-(1-7). The authors investigated receptor signalling via angiotensin type 1 and type 2 receptors (AT1R, AT2R) and Mas. The AT1R antagonist losartan blocked Ang II-induced, but not vasopressin-induced, hypertrophy. Losartan did not block the antihypertrophic effects of Ang-(1-9), or Ang-(1-7) on vasopressin-stimulated cardiomyocytes. The Mas antagonist A779 efficiently blocked the antihypertrophic effects of Ang-(1-7), without affecting Ang-(1-9). Furthermore, Ang-(1-7) activity was also inhibited in the presence of the bradykinin type 2 receptor antagonist HOE140, without affecting Ang-(1-9). Moreover, Flores-Muñoz et al. [56] observed that the AT2R antagonist PD123,319 abolished the antihypertrophic effects of Ang-(1-9), without affecting Ang-(1-7), suggesting Ang-(1-9) signals via the AT2R. Radioligand binding assays 8 International Journal of Hypertension demonstrated that Ang-(1-9) was able to bind the AT2R (pKi = 6.28 ± 0.1). The data indicate that ACE2/Ang-(1-9) axis, acting as a counterregulator of Ang II, is an effective, and possibly direct novel anticardiac hypertrophy axis.