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Cardiovascular Research Advance Access [Accepted Manuscript] published online on March 18, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp093
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.
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Angiopoietin-1 alters microvascular permeability coefficients in vivo via modification of endothelial glycocalyx

Andrew H.J. Salmon1,2, Christopher R. Neal1, Leslie M. Sage1, Catherine A. Glass1, Steven J. Harper1 and David O. Bates1

1 Microvascular Research Laboratories, Bristol Heart Institute, Department of Physiology and Pharmacology, University of Bristol
2 Academic Renal Unit, Department of Clinical Science @ North Bristol, University of Bristol

Name and address for correspondence: David Bates or Andrew Salmon, Microvascular Research Laboratories, Bristol Heart Institute, Department of Physiology and Pharmacology, Preclinical Veterinary School, Southwell Street, University of Bristol, Bristol, United Kingdom, Tel: 0044 117 928 8367, Fax: 0044 117 928 8151, Email: Dave.Bates{at}bris.ac.uk or andy.salmon{at}bristol.ac.uk

Aims: In this study, we wished to determine whether angiopoietin-1 (Ang1) modified the permeability coefficients of non-inflamed, intact continuous and fenestrated microvessels in vivo and to elucidate underlying cellular mechanisms.

Methods: Permeability coefficients were measured using the Landis-Michel technique (in frog and rat mesenteric microvessels) and an oncopressive permeability technique (in glomeruli).

Results: Ang1 decreased water permeability (LP: hydraulic conductivity) in continuous and fenestrated microvessels and increased retention of albumin ({sigma}: reflection coefficient) in continuous microvessels.

Endothelial glycocalyx is common to these anatomically distinct microvascular beds, and contributes to the magnitude of both LP and {sigma}. Ang1 treatment increased endothelial glycocalyx depth in intact microvessels and increased glycosaminoglycan content of cultured microvascular endothelial cell supernatant. Ang1 also prevented the pronase-induced increase in LP (attributable to selective removal of endothelial glycocalyx by pronase) by restoration of glycocalyx at the endothelial cell surface. The reduction in permeability was inhibited by a cell transport inhibitor, Brefeldin.

Conclusions: Ang1 modifies basal microvessel permeability coefficients, in keeping with previous reports demonstrating reduced solute flux in inflamed vessels. Anatomical, biochemical and physiological evidence indicates that modification of endothelial glycocalyx is a novel mechanism of action of Ang1 that contributes to these effects.

KEYWORDS permeability; angiopoietin-1; glycocalyx; microvessel; glomerulus

Time for primary review: 36 Days


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