Besides, in experimental hypertension (DOCA salt model) and in normotensive sham animals, RhoA/Rho-kinase inhibition (a signaling pathway that participates in pathological cardiovascular and renal remodeling and also in blood pressure regulation) by fasudil reduced BP and increased vascular and plasma ACE2 enzymatic activity. At the same time, fasudil reduced Ang II and increased Ang-(1-9) plasma levels ( Figure 2 ) [78] . No modifications were observed here in Ang-(1-7) levels despite increased ACE2 levels with RhoA/Rho-kinase inhibition [78] . Thus, RhoA/Rho-kinase inhibition, by increasing eNOS and/or by reducing both ACE and Ang II, does not activate the Ang-(1-7) pathway. This novel effect of RhoA/Rho-kinase inhibition on both ACE2 expression and Ang-(1-9) levels might additionally contribute to the antihypertensive effects of RhoA/Rhokinase inhibitors. Besides, these results strongly suggest that in this experimental model, hypertension is more dependent on ACE2 and Ang-(1-9) levels than on ACE and Ang II levels. Therefore, this second RAAS axis through ACE2 and Ang-(1-9) could be an important target for the treatment of hypertension.