Endogenous ATP Released by Electrical Field Stimulation Causes Contraction via P2x- and P2y-Purinoceptors in the Isolated Tail Artery of Rats

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Author(s)

    • HONDA Kenji
    • Department of Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
    • SAITO Ryo
    • Department of Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University
    • KAMIYA Hiro-o
    • Department of Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University

Abstract

Electrical field stimulation (EFS) caused contraction of isolated tail arteries of rats. The EFS-induced contraction showed frequency-dependence and was entirely abolished by the sodium channel blocker tetrodotoxin (1×10<SUP>-7</SUP> M). The EFS-induced (at 20 Hz) contraction was reduced by about 60% in the presence of phentolamine (1×10<SUP>-6</SUP> M). Therefore, later experiments were carried out in the presence of phentolamine. Pyridoxal-phosphate-6-azophenyl-2′, 4′-disulphonic acid (PPADS) (1×10<SUP>-8</SUP> - 1×10<SUP>-6</SUP> M) and basilen blue E-3G (3×10<SUP>-5</SUP> - 5×10<SUP>-5</SUP> M), P2-receptor antagonists, significantly inhibited the contraction evoked by EFS. In addition, PPADS significantly inhibited the contractions induced by ATP (1×10<SUP>-4</SUP> M) and a selective P2x-receptor agonist, α, β-methylene ATP (1×10<SUP>-6</SUP> M). In contrast, basilen blue E-3G did not inhibit α, β-methylene ATP-induced contraction. The ecto-ATPase activator apyrase (5 and 10 U/ml) significantly reduced the EFS-induced contractions. These findings suggest that endogenous ATP released by EFS causes contractions of rat tail artery via both the P2x-receptors and P2y-receptors.

Journal

  • The Japanese Journal of Pharmacology

    The Japanese Journal of Pharmacology 81(4), 375-380, 1999-12-01

    The Japanese Pharmacological Society

References:  30

Codes

  • NII Article ID (NAID)
    10008197687
  • NII NACSIS-CAT ID (NCID)
    AA00691188
  • Text Lang
    ENG
  • Article Type
    ART
  • ISSN
    00215198
  • NDL Article ID
    4948580
  • 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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