Skip Navigation


Cardiovascular Research Advance Access originally published online on December 10, 2008
Cardiovascular Research 2009 81(2):240-241; doi:10.1093/cvr/cvn342
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
81/2/240    most recent
cvn342v2
cvn342v1
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 Krötz, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Krötz, F.
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 2008. For permissions please email: journals.permissions@oxfordjournals.org

Putting the vasoactive effects of COX-2-derived prostanoids into clinical perspective

Florian Krötz

Cardiology Division, Medical Policlinic, Ludwig-Maximilians-University, Ziemssenstr. 1, 80336 München, Germany

Corresponding author. Tel: +49 89 5160 2111; fax: +49 89 5160 2410. E-mail address: florian.kroetz@med.uni-muenchen.de

This editorial refers to ‘Selective cyclooxygenase-2 inhibition directly increases human vascular reactivity to norepinephrine during acute inflammation’ by Foudi et al.,7 pp. 269–277, this issue.

The first 10% of the full text of this article appears below.

Ever since the recognition that the selective inhibitor of cyclooxygenase (COX)-2, rofecoxib, increases the risk for adverse cardiovascular events, enormous attention has been given to the mechanisms underlying these adverse vascular effects of the coxibs.1,2 Many recent studies that have investigated the biological consequences of COX-2 inhibition in the vasculature have focussed either on the prothrombotic side effects of decreased endothelial prostacyclin production during selective COX-2 blockade3,4 or on detrimental effects of such an intervention on atherosclerosis.5,6 Although such studies have greatly broadened our understanding of the pathophysiological roles of COX-2-mediated prostanoid production in vascular biology, the important vasodilatory functions of COX-2-derived prostanoids have been somewhat eclipsed by them.

. . . [Full Text of this Article]


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

Related Article

Selective cyclooxygenase-2 inhibition directly increases human vascular reactivity to norepinephrine during acute inflammation
Nabil Foudi, Liliane Louedec, Thierry Cachina, Charles Brink, and Xavier Norel
Cardiovasc Res 2009 81: 269-277. [Abstract] [Full Text] [PDF]