Structure and mechanical properties of resistance arteries in hypertension- Role of adhesion molecules and extracellular matrix determinants

Abnormalities of resistance arteries may play a role in the pathogenesis an d pathophysiology of hypertension in experimental animals and humans. Vesse ls that, when relaxed, measure <400 mu m in lumen diameter act as the major site of vascular resistance and include a network of small arteries (lumen approximate to 100 to 400 mu m) and arterioles (<100 mu m). Because increa sed peripheral resistance is generated by a narrowed lumen diameter, signif icant effort has been focused on determining the mechanisms that reduce lum en size. Three important vascular components are clearly involved, includin g alterations of vascular structure, mechanics (stiffness), and function. S tructural abnormalities comprise a reduced lumen diameter and thickening of the vascular media, resulting in an increased media-lumen ratio. Changes i n the mechanical properties of an artery, particularly increased stiffness, may also result in a reduced lumen diameter. These vascular abnormalities may be caused or influenced by the expression and/or topographic localizati on of extracellular matrix components, such as collagen and elastin, and by changes in cell-extracellular fibrillar attachment sites, such as adhesion molecules like integrins. This article discusses the abnormalities of resi stance arteries in hypertension and reviews the evidence suggesting an impo rtant role for adhesive and extracellular matrix determinants.