(Hypertension. 2000;36:312.)
© 2000 American Heart Association, Inc.
Brief Reviews |
From the Metabolic Research Unit (H.D.I.), University of California at San Francisco, and the MRC Multidisciplinary Research Group on Hypertension (E.L.S.), Clinical Research Institute of Montreal, Quebec, Canada.
Correspondence to Ernesto L. Schiffrin, MD, PhD, FRCPC, Clinical Research Institute of Montreal, 110 Pine Ave W, Montreal, Quebec, Canada H2W 1R7. E-mail schiffe{at}ircm.qc.ca
AbstractAbnormalities of
resistance arteries may play a role in the pathogenesis and
pathophysiology of hypertension in experimental animals and humans.
Vessels that, when relaxed, measure <400 µm in lumen diameter
act as the major site of vascular resistance and include a network of
small arteries (lumen
100 to 400 µm) and arterioles
(<100 µm). Because increased peripheral resistance
is generated by a narrowed lumen diameter, significant effort has been
focused on determining the mechanisms that reduce lumen size. Three
important vascular components are clearly involved, including
alterations of vascular structure, mechanics (stiffness), and function.
Structural abnormalities comprise a reduced lumen diameter and
thickening of the vascular media, resulting in an increased media-lumen
ratio. Changes in 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 localization 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 resistance arteries in
hypertension and reviews the evidence suggesting an important role for
adhesive and extracellular matrix determinants.
Key Words: remodeling resistance elasticity integrins hypertension, essential
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