Skip Navigation



European Heart Journal Advance Access published online on August 17, 2009
European Heart Journal, doi:10.1093/eurheartj/ehp330
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplementary Data
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 Gkaliagkousi, E.
Right arrow Articles by Ferro, A.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gkaliagkousi, E.
Right arrow Articles by Ferro, A.
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

Decreased platelet nitric oxide contributes to increased circulating monocyte-platelet aggregates in hypertension

Eugenia Gkaliagkousi1, Valerie Corrigall2, Silke Becker1, Patricia de Winter1, Ashish Shah1, Chrysanthos Zamboulis3, James Ritter1 and Albert Ferro1,*

1 Department of Clinical Pharmacology, Cardiovascular Division, King's College London, 3.07 Franklin-Wilkins Building, 150 Stamford Street, London SE1 9NH, UK
2 Department of Rheumatology, King's College London, Guy's Campus, London, UK
3 2nd Prop. Department of Medicine, Aristotle University of Thessaloniki, Thessaloniki, Greece

Received 19 January 2009; revised 22 April 2009; accepted 16 June 2009 * Corresponding author. Tel: +44 20 7848 4283, Fax: +44 20 7848 3743, Email: albert.ferro{at}kcl.ac.uk

Aims: The aim of this study was to determine the effect of blood pressure (BP) on platelet nitric oxide (NO) signalling and on formation of circulating monocyte-platelet aggregates (MPA), as well as the role of platelet NO in modulating MPA in hypertension.

Methods and results: We first examined platelet NO signalling in 23 untreated hypertensive (UH) and 23 normotensive (NT) subjects. Platelets from hypertensives exhibited reduced NO synthase activation by albuterol or collagen, as well as suppressed basal and stimulated NO-attributable cyclic guanosine-3',5'-monophosphate, compared with NT. In a second study, comprising 106 subjects with a wide BP range, circulating MPA showed a strong positive correlation with BP. On multiple regression analysis, using a model incorporating systolic BP (SBP), diastolic BP, age, lipids, gender, and smoking status, the only independent predictor of MPA was SBP. Nitric oxide synthase inhibition with NG-monomethyl-L-arginine increased MPA in NT but not in hypertensives, whereas the NO donor spermine NONOate (SNO) decreased MPA in NT but not in hypertensives. Platelet P-selectin expression was higher in hypertensives than in NT, and its expression was suppressed by SNO in NT only.

Conclusion: Platelet NO production and responsiveness are suppressed with raised BP, and this may contribute to the increase in platelet P-selectin and hence in circulating MPA in hypertension.

Key Words: Platelets • Monocytes • Monocyte-platelet aggregates • Nitric oxide • Blood pressure


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




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.