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Blood, 15 December 2006, Vol. 108, No. 13, pp. 4059-4062. Prepublished online as a Blood First Edition Paper on August 24, 2006; DOI 10.1182/blood-2006-02-005330. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-02-005330v1 108/13/4059    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Anning, P. B. Articles by O'Donnell, V. B. Search for Related Content PubMed PubMed Citation Articles by Anning, P. B. Articles by O'Donnell, V. B. Related Collections Signal Transduction Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Brief report Nitric oxide deficiency promotes vascular side effects of cyclooxygenase inhibitors Peter B. Anning, Barbara Coles, Jonathan Morton, Haibin Wang, Jashim Uddin, Jason D. Morrow, Sudhansu K. Dey, Lawrence J. Marnett, and Valerie B. O'Donnell From the Department of Medical Biochemistry and Immunology, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom; the Departments of Biochemistry and Chemistry, Vanderbilt Institute of Chemical Biology, Center in Molecular Toxicology, Vanderbilt-Ingram Cancer Center, Nashville, TN; and the Pediatrics, Cell, and Developmental Biology and Pharmacology, Vanderbilt University, Nashville, TN. The cardiovascular safety of COX-2 selective and nonselective nonsteroidal anti-inflammatory drugs (NSAIDs) has recently been called into question. The factors that predispose to adverse events by NSAIDs are unknown. Because patients with arthritis have decreased nitric oxide (NO) bioavailability, the in vivo effects of NSAIDs on murine vascular tone and platelet activity in the presence or absence of NO were examined. Here, we show that acute hypertensive and prothrombotic activities of the COX-2–selective inhibitor celecoxib are revealed only after in vivo inhibition of NO generation. The nonselective NSAID indomethacin was hypertensive but antithrombotic when NO was absent. In vitro myography of aortic rings confirmed that vasoconstriction required inhibition of both NOS and COX-2 and was abolished by supplementation with exogenous NO. These data indicate that NO suppresses vascular side effects of NSAIDs, suggesting that risk will be greatest in patients with impaired vascular function associated with decreased NO bioavailability. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Morton, B. Coles, K. Wright, A. Gallimore, J. D. Morrow, E. S. Terry, P. B. Anning, B. P. Morgan, V. Dioszeghy, H. Kuhn, et al. Circulating neutrophils maintain physiological blood pressure by suppressing bacteria and IFN{gamma}-dependent iNOS expression in the vasculature of healthy mice Blood, May 15, 2008; 111(10): 5187 - 5194. [Abstract] [Full Text] [PDF]

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