The protein and mRNA of ACE2 are expressed in human coronary arteries and arterioles and the vasa vasorum of most organs [9, 91] . Recently, ACE2 expression has also been (1-7) , Ang-(1-9) and Ang II in DOCA salt hypertensive rats treated with the Rho kinase inhibitor fasudil. Increased plasma levels of Ang-(1-9) were observed in DOCA salt hypertensive rats treated with the Rho kinase inhibitor fasudil. Fasudil (100 mh/kg/day) by gavage was administered during 3 weeks, starting on the third week after DOCA administration. Data are presented as mean ± SEM (n = 8-11/group). DOCA: deoxycorticosterone, F: fasudil. * P < 0.05 compared to both Sham and untreated DOCA groups (adapted with permission from [78] ). observed in the large conduit arteries (aorta and carotid) in the HR [92] . ACE2 localizes preferentially in endothelial cells and arterial smooth muscle cells (SMCs) [9, 91] . As for the role of ACE2 in vascular remodeling, the effect of ACE2 on neointima formation has not yet been studied, but Ang-(1-7) infusion after balloon-catheter injury of the rat carotid artery reduced neointima formation [93] . This effect was probably mediated by its inhibition of vascular SMC proliferation [94] . In hypertensive animal models, ACE2 mRNA and protein were associated with immunoreactive Ang-(1-7) in the large conduit arteries of SHRs. Treatment with an ARB induced a fivefold increase in ACE2 mRNA and was associated with a significant increase in aortic Ang-(1-7) protein expression. This effect was associated with a decrease in aortic medial thickness, suggesting that this may be a protective mechanism in the prevention of cardiovascular events during hypertension [94] . Igase et al. [95] showed that ACE2 protein is expressed not only in the media of the carotid artery but also in the neointima of the ballooninjured carotid artery in SHR. The increase in ACE2 protein expression in the neointima following exposure of the rats to an ARB compared to vehicle was associated with a reduction in neointima thickness. These results lead to the hypothesis that there is a strong correlation between the increase in ACE2 protein in the injured carotid artery of SHR and vascular remodeling during blockade of Ang II receptors [95] .