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Wall Tissue Remodeling Regulates Longitudinal Tension in Arteries

From The Toronto General Research Institute, University Health Network, and the Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada.

Correspondence to Lowell Langille, PhD, Toronto General Hospital, University Health Network, 200 Elizabeth St, CCRW 1-836, Toronto, Canada M5G 2C4. E-mail langille{at}uhnres.utoronto.ca

Changes in blood pressure or flow induce arterial remodeling that normalizes mechanical loads that are imposed on arterial tissue. Arteries are also under substantial longitudinal stretch (axial strain) that may be altered by growth or atrophy of tissues to which they are attached. We therefore tested whether axial strain is also regulated in a negative feedback manner through arterial remodeling. Axial strain in rabbit carotid arteries was increased from 62±2% to 97±2% without altering other mechanical loads on wall tissues. Strain was reduced within 3 days and completely normalized by 7 days. Remodeling involved tissue elaboration, endothelial cell replication rates were increased by >50-fold and smooth muscle cell replication rates were increased by >15-fold, and substantially elevated DNA, elastin, and collagen contents were recorded. Also, increased rates of apoptosis were indicated by degradation of DNA into oligonucleosomes, and matrix remodeling was reflected in enlarged fenestrae in the internal elastic lamina and increased expression and activation of gelatinases, especially matrix metalloproteinase-2. Intriguingly, reduced axial strain was not normalized, presumably because remodeling processes, apart from cell contraction, are ineffective in decreasing strain, and arterial smooth muscle orientation precludes large effects of contraction on axial strain.

Key Words: remodeling • axial strain • extracellular matrix • proliferation • apoptosis

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