So far, all attention has been focused on Ang- (1-7) , that opposes the pressor, proliferative, profibrotic, and prothrombotic actions mediated by Ang II [76] . Experimental and clinical studies have demonstrated a role for the Ang-(1-7)/ACE2/Mas axis in the evolution of hypertension, the regulation of cardiovascular and renal function, and the progression of cardiovascular and renal disease including diabetic nephropathy [77] . Additional evidence suggests that a reduction in the expression and activity of this vasodepressor component may be a critical factor in mediating the progression of cardiovascular and renal disease. These findings support a role for the Ang-(1-7)/ACE2/Mas axis and, in particular, on its putative role as an ACE-Ang II-AT1 receptor counter-regulatory axis within the RAS [76, 77] .