Hypertensive Vasculopathy

Abstract

Essential hypertension is characterized by an increase in total peripheral vascular resistance, due primarily to a decrease in lumen diameter and an increase in media thickness. Underlying these phenomena are altered vascular tone (decreased relaxation and/or increased contraction) and structural remodeling. Endothelial dysfunction and arterial remodeling characterize the vascular phenotype of hypertension, known as “hypertensive vasculopathy.” Initial factors contributing to vasculopathy of hypertension involve increased transmural pressure, changes in blood flow, impaired endothelial function, and altered vascular smooth muscle cell (VSMC) contractility. More chronic changes are associated with perturbed VSMC growth, migration, differentiation, calcification and inflammation, and production of extracellular matrix proteins, responsible for structural remodeling. At the level of the vascular cells, receptors are activated by vasoactive agents and mechanical forces triggering intracellular signaling pathways and generation of reactive oxygen species (ROS). These subcellular events underlie VSMC dedifferentiation, realignment, calcification, and growth and stimulate inflammation, fibrosis, and osteogenic transformation, which contribute to endothelial dysfunction and thickening of the vascular wall. Such changes play a major role in the vasculopathy of hypertension.