The vascular wall is continuously exposed to hemodynamic forces such as the luminal pressure and shear stress. Changes in these forces, either physiological or pathological, lead to functional and/or structural alterations of the vascular wall [79] . Acute changes in hemodynamic forces can modify vessel diameter. Chronic changes in hemodynamic forces result in structural alterations of the vessel wall, indicated by changes in wall diameter and thickness. In addition, changes in vascular structure are not solely determined by hemodynamic forces [80] , but also by inflammatory responses and changes in extracellular matrix components [81] . Structural changes of the medial layer of the vascular wall during hypertension are termed "eutrophic remodeling" [82] and subsequently translate to other vascular pathologies. This involves an inward encroachment of the arterial wall thereby, reducing the diameter of the lumen [83] . Several RAAS components are involved in neointimal formation after vascular endothelial damage [84] . In particular, Rakugi et al. [85] observed that vascular endothelial damage results in the induction of vascular ACE. Their results suggested that inhibition of vascular ACE might be critical in the prevention of restenosis after balloon injury. Patients with previously untreated essential hypertension and eutrophic inward remodeling appears to respond to antihypertensive medication. Reduction in BP with drugs that block the RAAS such as ACEIs [86] [87] [88] or ARBs [86, 87, 89] and calcium channel antagonists [90] are able to reverse the eutrophic inward remodeling [88] .