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Cardiovascular Research Advance Access first published online on March 18, 2008
This version [Corrected Proof] published online on April 9, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn080
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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 nitric oxide identified in vivo through spectral analysis

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

1 Unit of Pharmacology and Therapeutics, Université catholique de Louvain, UCL-FATH 5349, Vésale+5, 52 Avenue Mounier, 1200 Brussels, Belgium
2 Unit of Biomedical Imaging Resonance, Université catholique de Louvain, Brussels, Belgium

* Corresponding author. Tel: +32 2 764 5260; fax: +32 2 762 5269.E-mail address: 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, a key regulator of blood pressure (BP). However, the impact of genetic alteration of cav-1 on vascular nitric oxide (NO) production and BP homeostasis in vivo is unknown.

Methods and results: We used spectral analysis of systolic blood pressure (SBP) 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. 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 SBP levels. Conversely, VLF variability was increased upon acute injection of mice, with a peptide containing the caveolin-scaffolding domain (CSD; residues 82–101) fused to an internalization sequence of antennapedia that decreased vascular and circulating NO in vivo.

Conclusion: 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, pharmacological, or molecular interventions that modulate cav-1 expression in diseases with NO-dependent endothelial dysfunction.

KEYWORDS Blood pressure; Blood pressure variability; Nitric oxide; Caveolin-1; Endothelial function

Time for primary review: 27 days

{dagger} These two authors contributed equally.


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