Premium
Shear stress Lp response enhanced by chondroitin sulfate and hyaluronic acid is Rho kinase dependent
Author(s) -
Adamson R H,
Sarai R K,
Altangerel A,
Clark J F,
Curry F E
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.975.14
Subject(s) - glycocalyx , hyaluronic acid , chemistry , perfusion , shear stress , chondroitin sulfate , bovine serum albumin , biophysics , glycosaminoglycan , biochemistry , anatomy , materials science , medicine , biology , composite material
Vascular endothelial cells (EC) orient their long axes parallel to the fluid flow direction both in vivo and in culture. The surface glycocalyx of cultured EC transduces the fluid flow shear stress that mediates nitric oxide production and EC cytoskeletal rearrangement (Thi et al., PNAS 2004 101(47): 16483). Previously we showed that for intact microvessels perfusion against the normal flow direction stimulated increased hydraulic permeability (L p ) correlated with shear stress and induced rearrangement of cytoskeletal structures using Ringer's solution containing bovine serum albumin (BSA; 10 mg/ml) as perfusate. As a further test we added chondroitin sulfate (C; 0.2 mg/ml) and hyaluronic acid (H; 0.2 mg/ml) to the perfusate (CH; to maintain glycocalyx structure; Potter & Damiano, Circ Res 2008; 102:770) and we measured L p in rat mesentery venular microvessels perfused for 2 hours against the normal flow direction (Reverse). Reverse perfused CH vessels had a mean Lp change (ΔLp) of 18 ± 9 ( sem ; ×10 −7 cm/(s×cmH 2 O)) while for Reverse perfused BSA vessels ΔLp was 7.1 ± 3.5. Forward perfusion did not change Lp in either group. For Reverse perfusion using CH and the Rho kinase inhibitor Y27632 (30 μM) ΔLp was 6.2 ± 3.5. The data suggest that CH helps maintain an intact glycocalyx which is more sensitive to altered shear stress than that of BSA perfused vessels and that the ΔLp response is Rho kinase dependent. Supp NIH HL44485.