Rarefaction is another type of remodeling that is found in hypertension. It occurs at the level of small arterioles with a lumen diameter smaller than 40 μm and capillaries [1]. With rarefaction, the density of arterioles and capillaries in tissues is diminished and consequently vascular resistance is increased [72, 73] and tissue perfusion is impaired [74]. Arteriolar rarefaction is functional initially as a result of vasoconstriction, and later anatomical and permanent, followed by rarefaction of capillaries with decreased tissue perfusion. Decreases in tissue perfusion have been associated with vascular complications and cardiovascular events [75].

Vascular remodeling and endothelial dysfunction in small resistance arteries are features regularly reported in hypertension. Functional, structural, and mechanical alterations of resistance arteries are probably the earliest alterations in the vasculature found in hypertensive subjects younger than 60 years of age. They take the form of eutrophic inward remodeling accompanied by endothelial dysfunction associated eventually to enhanced stiffness. These changes have been shown to have prognostic significance with respect to outcomes. They could contribute through wave reflection to increases in stiffness of large arteries and thus to systolic hypertension and the increased pulse pressure found in older subjects with hypertension. Alternatively, increased large artery stiffness could increase pulsatility, which when conducted into the microcirculation, may cause injury and remodeling of small arteries and arterioles. Activation of the RAAS plays a key role in vascular remodeling and endothelial dysfunction through redox-sensitive pathways that promote growth and inflammation in the blood vessel wall.