Involvement of Adenosine A_2 Receptors in the Changes of Tissue Factor-Dependent Coagulant Activity Induced by Polymorphonuclear Leukocytes in Endothelial Cells

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Author(s)

Abstract

We have already reported that polymorphonuclear leukocytes (PMNs) could increase tissue factor-dependent coagulant activity (TF activity) in endothelial cells mediated by adhesion of PMNs to endothelial cells. In the present study, the role of adenosine receptors in the changes of TF activity and of adhesion between PMNs and endothelial cells was examined. The increases of the TF activity and adhesion were significantly reduced in a concentration-dependent manner by pretreatment of adenosine (0.1 and 1.0 mM); an adenosine A<sub>1</sub>/A<sub>2</sub>-receptor agonist, CGS-21680 (5, 10 and 50 μM); and an adenosine A<sub>2</sub>-receptor agonist, 5'-(<i>N</i>-cyclopropyl)-carboxamidoadenosine (CPCA; 1.0, 10 and 100 nM). An adenosine A<sub>2</sub>-receptor antagonist, 3,7-dimethyl-1-(2-propynyl) xanthine (DMPX; 1.0 and 100 nM), antagonized significantly the reduction of the TF activity and the adhesion induced by adenosine (1.0 mM), while 8-cyclopentyl-1,3-dimethylxanthine (CPDMX; 1.0 and 100 nM), an adenosine A<sub>1</sub>-receptor antagonist, did not affect it. On the other hand, the TF activity and the adhesion were not changed by <i>N</i><sup>6</sup>-cyclohexyladenosine (CHA; 10 and 100 nM) and 2-chloro-<i>N</i>-cyclopentyladenosine (CCPA; 10 and 100 nM), adenosine A<sub>1</sub>-receptor agonists in the same conditions. These results suggest that the reduction in the TF activity stimulated by PMNs is closely related to the adhesive inhibition between PMNs and endothelial cells through the adenosine A<sub>2</sub>-receptor-mediated system.

Journal

  • The Japanese Journal of Pharmacology

    The Japanese Journal of Pharmacology 88(4), 407-413, 2002-04-01

    The Japanese Pharmacological Society

References:  27

Codes

  • NII Article ID (NAID)
    10008415103
  • NII NACSIS-CAT ID (NCID)
    AA00691188
  • Text Lang
    ENG
  • Article Type
    ART
  • ISSN
    00215198
  • NDL Article ID
    6263208
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z53-D199
  • Data Source
    CJP  NDL  J-STAGE 
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