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Thromb Haemost 1997; 78(04): 1268-1271
DOI: 10.1055/s-0038-1657726
Rapid Communication
Schattauer GmbH Stuttgart

Partial Blockade of Nitric Oxide Synthase Blunts the Exercise-induced Increase of von Willebrand Factor Antigen and of Factor VIII in Man

Authors

  • Bernd Jilma

    1   The Department of Clinical Pharmacology, University of Vienna, Austria

  • Eva Dirnberger

    1   The Department of Clinical Pharmacology, University of Vienna, Austria

  • Hans-Georg Eichler

    1   The Department of Clinical Pharmacology, University of Vienna, Austria

  • Bettina Matulla

    1   The Department of Clinical Pharmacology, University of Vienna, Austria

  • Leopold Schmetterer

    1   The Department of Clinical Pharmacology, University of Vienna, Austria
    2   The Institute of Medical Physics, University of Vienna, Austria

  • Stylianos Kapiotis

    3   The Clinical Department of Medical and Chemical Laboratory Diagnostics, Vienna University Hospital School of Medicine, Austria

  • Wolfgang Speiser

    3   The Clinical Department of Medical and Chemical Laboratory Diagnostics, Vienna University Hospital School of Medicine, Austria

  • Oswald F Wagner

    3   The Clinical Department of Medical and Chemical Laboratory Diagnostics, Vienna University Hospital School of Medicine, Austria
Further Information

Publication History

Received 07 1997

Accepted after revision 02 July 1997

Publication Date:
12 July 2018 (online)

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Summary

Background: Until now the effects of β-adrenergic agonists have largely been ascribed to their ability to induce intracellular formation of cyclic adenosine monophosphate. Recently evidence has been accumulating that at least some β1 and β2-adrenoceptor effects may be mediated by nitric oxide (NO). Based on these studies, we hypothesized that the β-adrenoceptor mediated increase of von Willebrand factor and factor VIII-activity (FVIII:C) in plasma during exercise, is caused by an NO-dependent mechanism. Methods: Thirteen young healthy subjects finished an exhaustive bicycle exercise protocol while they were infused placebo or the NO-synthase inhibitor N-monomethyl-L-arginine (L-NMMA) on two separate days in a randomized, double blind cross-over design. Findings: During exercise systemic haemo-dynamic changes were parallel in both treatment periods, but L-NMMA caused a partial inhibition of NO-synthase as evidenced by a 30% decrease in exhaled NO. The workload capacities were not different during L-NMMA or placebo infusion. However, under placebo treatment exercise increased vWF-Ag by a maximum of 61% (CI: 43-84; p = 0.002) and FVIII:C by 44% (CI: 31-59; p = 0.001), which was significantly attenuated when subjects were treated with L-NMMA (p <0.05): under L-NMMA treatment vWF-Ag increased by only 25% (CI: 5-51; p = 0.001) and FVIII:C by 12% (CI: 6-39; p = 0.001). Interpretation: Partial blockade of NO-synthase with L-NMMA blunts the exercise-induced increase in vWF-Ag and FVIII:C. Our trial points to a role of endogenous NO-generation in the β2-adrenergic increase in vWF/FVIII. Thus, we propose that physiologic processes which are induced by systemic β2-adrenoceptor stimulation may at least partly be mediated by NO.