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Hypertension. 2008;52:195-200
Published online before print June 9, 2008, doi: 10.1161/HYPERTENSIONAHA.107.103440
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(Hypertension. 2008;52:195.)
© 2008 American Heart Association, Inc.


Brief Reviews

Mechanisms of Arterial Remodeling in Hypertension

Coupled Roles of Wall Shear and Intramural Stress

Jay D. Humphrey

From the Department of Biomedical Engineering, Texas A&M University, College Station.

Correspondence to Jay D. Humphrey, Department of Biomedical Engineering, 337 Zachry Engineering Center, 3120 TAMU, Texas A&M University, College Station, TX 77843-3120. E-mail jhumphrey@tamu.edu


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 


*    Introduction
 
Diverse data collected over the past 4 decades suggest the existence of a mechanical homeostasis across multiple length and time scales in the vasculature. For example,1 stress fibers within endothelial and vascular smooth muscle cells appear to disassemble and then reassemble in a mechanically preferred manner when perturbed from a normal value of mechanical stress or strain; focal adhesions in smooth muscle cells and fibroblasts tend to increase in area in response to local increases in mechanical loading so as to maintain the stress constant at a preferred value; fibroblasts tend to increase the tractions that they exert on the extracellular matrix when external loads are decreased from a preferred value, thus suggesting an attempt to enforce a "tensional homeostasis"; vascular smooth muscle cells tend to relengthen to their normal, preferred values when an arteriole is forced into a vasoconstricted state for an extended period; and arteries tend to decrease in caliber in response to sustained decreases in flow-induced wall shear stress, to increase in thickness in response to sustained increases in pressure-induced circumferential stress, and to lengthen in response to extension-induced increases in axial stress. Although changes in the cytoskeleton and integrins occur within minutes, changes at the cell-cell and cell-matrix levels occur over hours, and those at the vessel level occur over days to weeks or months. Hence, despite marked differences in length scales (dimensions from nanometers to centimeters) and time scales (durations from minutes to months), mechanobiological control mechanisms in the vasculature tend to restore values of . . . [Full Text of this Article]




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