Skip Navigation



Cardiovascular Research Advance Access [Accepted Manuscript] published online on March 18, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn080
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Data
Right arrow All Versions of this Article:
79/3/527    most recent
cvn080v2
cvn080v1
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 arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Desjardins, F.
Right arrow Articles by Balligand, J.-L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Desjardins, F.
Right arrow Articles by Balligand, J.-L.
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 2008. For permissions please email: journals.permissions@oxfordjournals.org

Control of blood pressure variability in caveolin-1-deficient mice: role of NO identified in vivo through spectral analysis

Fanny Desjardins1, Irina Lobysheva1, Michel Pelat1, Bernard Gallez2, Olivier Feron1, Chantal Dessy1,# and Jean-Luc Balligand1,#,*

1 Unit of Pharmacology and Therapeutics, Université catholique de Louvain, Brussels, Belgium
2 Unit of Biomedical Imaging Resonance, Université catholique de Louvain, Brussels, Belgium

* Correspondence to J-L Balligand, MD, PhD; UCL-FATH 5349, Vésale+5, 52 Avenue Mounier, 1200 Brussels, Belgium, Phone: +32-2-764 5260, Fax: +32-2-762-5269 Balligand{at}mint.ucl.ac.be

Aims: In endothelial cells, caveolin-1 (cav-1) is known to negatively modulate the activation of endothelial nitric oxide synthase (eNOS), a key regulator of blood pressure (BP). However, the impact of genetic alteration of cav-1 on vascular NO production and BP homeostasis in vivo is unknown.

Methods: We used spectral analysis of systolic BP variability in mice chronically equipped with telemetry implants to identify frequency ranges (0.05-0.4 Hz, very-low-frequency;VLF) specifically responding to NO, independently of changes in absolute BP or systemic neurohormone levels.

Results: VLF variability was inversely correlated to aortic vasodilator-stimulated Ser239 phosphoprotein (VASP) phosphorylation, reflecting NO bioactivity. We show that mice deficient in cav-1 have decreased VLF variability paralleled with enhanced systemic and vascular production of NO at unchanged mean systolic BP levels. Conversely, VLF variability was increased upon acute injection of mice with a peptide containing the caveolin-scaffolding domain (residues 82-101;CSD) fused to an internalization sequence of Antennapedia that decreased vascular and circulating NO in vivo.

Conclusions: These data highlight the functional importance of cav-1 for the production of bioactive NO in conduit arteries and its control of central BP variability. Given the impact of the latter on target organ damage, this raises the interest for genetic, pharmacologic or molecular interventions that modulate cav-1 expression in diseases with NO-dependent endothelial dysfunction.

Time for primary review: 27 days

# contributed equally


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


This article has been cited by other articles:


Home page
 Physiol. Rev.Home page
J.-L. Balligand, O. Feron, and C. Dessy
eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues
Physiol Rev, April 1, 2009; 89(2): 481 - 534.
[Abstract] [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.