Skip Navigation


Cardiovascular Research Advance Access first published online on March 18, 2009
This version [Corrected Proof] published online on April 23, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp093
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Data
Right arrowOA All Versions of this Article:
83/1/24    most recent
cvp093v3
cvp093v2
cvp093v1
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Salmon, A. H.J.
Right arrow Articles by Bates, D. O.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Salmon, A. H.J.
Right arrow Articles by Bates, D. O.
Related Collections
Right arrowRelated Article
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.

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 Department of Physiology and Pharmacology, Preclinical Veterinary School, Microvascular Research Laboratories, Bristol Heart Institute, University of Bristol, Southwell Street, Bristol BS2 8EJ, UK
2 Academic Renal Unit, Department of Clinical Science @ North Bristol, University of Bristol, Bristol, UK

* Corresponding author. Tel: +44 117 928 9818; fax: +44 117 928 8151. E-mail address: dave.bates{at}bris.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 the underlying cellular mechanisms.

Methods and results: Permeability coefficients were measured using the Landis–Michel technique (in frog and rat mesenteric microvessels) and an oncopressive permeability technique (in glomeruli). Ang1 decreased water permeability (LP: hydraulic conductivity) in continuous and fenestrated microvessels and increased the 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 the depth of endothelial glycocalyx in intact microvessels and increased the content of glycosaminoglycan 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.

Conclusion: 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: 37 days

The original version was incorrect. The lettering of Figure 3C and Figure 3D has been reversed. The publisher apologises for the error.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?

Related Article

Beyond tie-ing up endothelial adhesion: new insights into the action of angiopoietin-1 in regulation of microvessel permeability
Pingnian He
Cardiovasc Res 2009 83: 1-2. [Extract] [Full Text] [PDF]



This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
P. He
Beyond tie-ing up endothelial adhesion: new insights into the action of angiopoietin-1 in regulation of microvessel permeability
Cardiovasc Res, July 1, 2009; 83(1): 1 - 2.
[Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.