In vessels, new members of the RAS have been detected, including ACE2, Ang-(1-7) and Mas. Vascular ACE2 is functionally active and generates Ang-(1-7) from Ang II. Ang-(1-7) is found in the endothelium and vascular wall [101] [102] [103] and immunohistochemical staining shows abundant presence in aortic perivascular adventitial tissue [104, 105] . Ang- (1-7) , by binding to receptor Mas on endothelial cells, opposes Ang II actions by mediating vasodilation, growthinhibition, antiinflammatory responses, antiarrhythmogenic and antithrombotic effects [33, 68] through NOS-derived NO production, activation of protein tyrosine phosphatases, reduced MAPK activation and inhibition of NADPH oxidase-derived generation of reactive oxygen species (ROS) [106, 107] . Overexpression of ACE2 in the vascular wall of SHR is associated with improved endothelial function and attenuated development of hypertension [68] . Ang-(1-7)-Mas can hetero-oligomerize with AT1R, thereby inhibiting Ang II actions. The ACE2/Ang-(1-7)-Mas axis is now considered as a counter-regulatory system to the ACE-Ang II-AT1R axis in the vasculature [107] , although some evidence indicates that Ang-(1-7) may also promote fibrosis and inflammation in certain conditions [108, 109] .