Hypertensive vascular disease

Elevated blood pressure has an impact on the vasculature as a consequence of both the mechanical effects of blood pressure and shear stress, as well as the action of hormonal systems such as the renin–angiotensin–aldosterone system, endothelins, catecholamines, agents generated in perivascular fat, inflammatory mediators, such as different cytokines and chemokines, as well as immune mediators, such as lymphocytes and macrophages and their products. The vascular phenotype of hypertension varies according to the age of subjects. In younger individuals with elevated blood pressure, vascular remodeling occurs in small arteries and arterioles, and is usually eutrophic with a reduced lumen diameter and normal media cross-section, reduced or enhanced stiffness and increased extracellular matrix deposition, and associated, with the passage of time with endothelial dysfunction. In severe or advanced hypertension, and in secondary forms and refractory hypertension, hypertrophic vascular remodeling of small arteries and arterioles may be found. As blood pressure remains elevated for a prolonged time, or in subjects older than 50–55 years of age, vascular changes occur predominantly in large, conduit arteries, such as the aorta, which becomes stiffer as arteriosclerosis develops, resulting in increased pulse pressure. There occurs in a degree that depends on associated cardiovascular risk factors, progression of atherosclerosis, an inflammatory accumulation of lipids in plaques in the intima, triggered in part by endothelial dysfunction, dyslipidemia, age, smoking and diabetes. The vascular disease of hypertension, by promoting tissue underperfusion and progression of atherosclerosis, contributes to myocardial ischemia and cardiovascular events, heart failure, stroke, nephrosclerosis and chronic kidney disease and peripheral vascular disease.