The endothelial glycocalyx mediates shear-induced changes in hydraulic conductivity

被引:53
|
作者
Lopez-Quintero, Sandra V. [1 ]
Amaya, Ronny [1 ]
Pahakis, Manolis [1 ]
Tarbell, John M. [1 ]
机构
[1] CUNY City Coll, Dept Biomed Engn, New York, NY 10031 USA
关键词
endothelium; nitric oxide; shear stress; NITRIC-OXIDE; INDUCED INCREASE; CAROTID-ARTERY; L-P; STRESS; MONOLAYERS; PRESSURE; CELLS; MECHANOTRANSDUCTION; PERMEABILITY;
D O I
10.1152/ajpheart.00894.2008
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Lopez-Quintero SV, Amaya R, Pahakis M, Tarbell JM. The endothelial glycocalyx mediates shear-induced changes in hydraulic conductivity. Am J Physiol Heart Circ Physiol 296: H1451-H1456, 2009. First published March 13, 2009; doi:10.1152/ajpheart.00894.2008.-Recent in vitro and in vivo studies have reported fluid shear stress-induced increases in endothelial layer hydraulic conductivity (L-p) that are mediated by an increased production of nitric oxide (NO). Other recent studies have shown that NO induction by shear stress is mediated by the glycocalyx that decorates the surface of endothelial cells. Here we find that a selective depletion of the major components of the glycocalyx with enzymes can block the shear stress-induced response of L-p. Heparinase and hyaluronidase block shear-induced increases in L-p, which is consistent with their effects on NO production. But chondroitinase, which does not suppress shear-induced NO production, also inhibits shear-induced L-p. A further surprise is that treatment with the general proteolytic enzyme pronase does not suppress the shear L-p response. We also find that heparinase does not alter baseline L-p significantly, whereas chondroitinase, hyaluronidase, and pronase increase it significantly.
引用
收藏
页码:H1451 / H1456
页数:6
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