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Blood, 15 October 2005, Vol. 106, No. 8, pp. 2737-2743. Prepublished online as a Blood First Edition Paper on June 23, 2005; DOI 10.1182/blood-2005-02-0664. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-02-0664v1 2005-02-0664v2 106/8/2737    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 Williams, P. C. Articles by O'Donnell, V. B. Search for Related Content PubMed PubMed Citation Articles by Williams, P. C. Articles by O'Donnell, V. B. Related Collections Hemostasis, Thrombosis, and Vascular Biology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY In vivo aspirin supplementation inhibits nitric oxide consumption by human platelets P. Claire Williams, Marcus J. Coffey, Barbara Coles, Stephanie Sanchez, Jason D. Morrow, John R. Cockcroft, Malcolm J. Lewis, and Valerie B. O'Donnell From the Department of Medical Biochemistry and Immunology, School of Medicine, Cardiff University, Cardiff, United Kingdom; the Department of Cardiology, School of Medicine, Cardiff University, Cardiff, United Kingdom; the Department of Pharmacology, Therapeutics, and Toxicology, School of Medicine, Cardiff University, Cardiff, United Kingdom; and the Division of Pharmacology, Vanderbilt University Medical Center, Nashville, TN. Antiplatelet therapies improve endothelial function in atherosclerosis, suggesting that platelets regulate vascular nitric oxide (NO) bioactivity in vivo. Herein, washed platelets consumed NO on activation in an aspirin-sensitive manner, and aspirin enhanced platelet NO responses in vitro. To examine whether in vivo aspirin can inhibit platelet NO consumption, a double-blind placebo-controlled study was conducted. After a 2-week nonsteroidal anti-inflammatory drug (NSAID)–free period, healthy men were randomly assigned and administered aspirin (75 mg/d orally) or identical placebo for 14 days, then crossed over to the opposite arm. Following in vivo aspirin, NO consumption by platelets was inhibited 91%. Rate of onset and recovery following aspirin withdrawal was consistent with cyclooxygenase 1 (COX-1) inhibition. In a small substudy, NO consumption by platelets from postmenopausal women was faster in hypercholesterolemics and less sensitive to aspirin (ie, 39% versus 76% inhibition for hypercholesterolemics or normocholesterolemics, respectively). However, 150 mg aspirin/day increased inhibition of NO consumption by platelets of hypercholesterolemics to 80%. Comparisons of platelet COX-1 or -2 expression and urinary 11-dehydro-thromboxane B2 excretion suggested that aspirin was less able to block platelet activation in vivo in hypercholesterolemia. In conclusion, aspirin inhibits NO consumption by platelets from healthy subjects, but its beneficial effects on NO bioactivity may be compromised in some hypercholesterolemic patients. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: H. Bulckaen, G. Prevost, E. Boulanger, G. Robitaille, V. Roquet, C. Gaxatte, G. Garcon, B. Corman, P. Gosset, P. Shirali, et al. Low-dose aspirin prevents age-related endothelial dysfunction in a mouse model of physiological aging Am J Physiol Heart Circ Physiol, April 1, 2008; 294(4): H1562 - H1570. [Abstract] [Full Text] [PDF] G. Davi and C. Patrono Platelet Activation and Atherothrombosis N. Engl. J. Med., December 13, 2007; 357(24): 2482 - 2494. [Full Text] [PDF]

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