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Research ArticleCARDIOVASCULAR

Heterogenous Vascular Effects of AP5A in Different Rat Resistance Arteries Are Due to Heterogenous Distribution of P2X and P2Y1 Purinoceptors

Martin Steinmetz, Stefan Bierer, Peter Hollah, Karl Heinz Rahn and Eberhard Schlatter
Journal of Pharmacology and Experimental Therapeutics September 2000, 294 (3) 1182-1187;
Martin Steinmetz
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Stefan Bierer
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Peter Hollah
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Karl Heinz Rahn
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Eberhard Schlatter
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Abstract

In the accompanying article, we showed that AP5A displayed heterogenous vasoactive effects in rat resistance arteries. It induced a stable vasoconstriction in the superior epigastric artery (SEA) and a transient vasoconstriction in the mesenteric resistance artery (MrA). In the phenylephrine-precontracted MrA AP5A induced a marked vasorelaxation. In this study the noncompetitive inhibition of the AP5A-induced vasoconstriction with pyridoxal-phosphate-6-azophenyl-2′,4′-disulphonic acid was found to be significantly stronger in MrA than in SEA. The nonselective P2 purinoceptor antagonist suramin inhibited AP5A-induced vasoconstriction in MrA only. The vasoconstriction by the P2X purinoceptor agonist α,β-methylene ATP was inhibited by with pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonic acid and suramin similarly to that induced by AP5A. Thus, the AP5A-induced vasoconstriction is due to P2X receptor activation, but two different P2X receptors seem to be operational in the two different vessels. The AP5A-induced vasorelaxation of phenylephrine-precontracted MrA was inhibited by the P2Y1 receptor antagonist ADP3′5′. The vasorelaxation induced by ADPβS (P2Y1 agonist) also was inhibited by ADP3′5′. These findings suggest that AP5A-induced vasorelaxation of MrA is caused by P2Y1 receptor activation. The P1 (A2) receptor antagonist 3,7-dimethyl-1-propargylxanthine only slightly inhibited AP5A-induced vasorelaxation at high concentrations. Adenosine and the A2receptor agonist CGS21680 failed to produce significant vasorelaxation. Therefore, vasorelaxation in MrA does not involve A2purinoceptor activation. AP5A-induced vasorelaxation was not inhibited by Ca2+- or ATP-dependent K+ channel blockade with clotrimazole, apamin, or glibenclamide. These data indicate that vasoconstriction in MrA and SEA by AP5A is due to different P2X receptors, and vasorelaxation in precontracted MrA is due to P2Y1 receptor activation.

Footnotes

  • Send reprint requests to: Dr. M. Steinmetz, Medizinische Poliklinik, Westfälische Wilhelms-Universität Münster, Albert-Schweitzer-Strasse 33, 48129 Münster, Germany. E-mail: steinme{at}uni-muenster.de

  • ↵1 This study was supported by a grant of the Center for Interdisciplinary Clinical Research (IZKF, project A1) at the Medical Faculty of the University of Münster (BMBF 01 KS 9604/0).

  • Abbreviations:
    AP5A
    P1,P5-diadenosine pentaphosphate
    APnA
    diadenosine polyphosphates
    SEA
    superior epigastric artery
    MrA
    mesenteric resistance artery
    α,β-meATP
    α,β-methylene ATP
    PPADS
    pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid
    DMPX
    3,7-dimethyl-1-propargylxanthine
    DPCPX
    8-cyclopentyl-1,3-dipropylxanthine
    KRB
    Krebs-Ringer-bicarbonate solution
    • Received February 14, 2000.
    • Accepted May 4, 2000.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 294 (3)
Journal of Pharmacology and Experimental Therapeutics
Vol. 294, Issue 3
1 Sep 2000
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Research ArticleCARDIOVASCULAR

Heterogenous Vascular Effects of AP5A in Different Rat Resistance Arteries Are Due to Heterogenous Distribution of P2X and P2Y1 Purinoceptors

Martin Steinmetz, Stefan Bierer, Peter Hollah, Karl Heinz Rahn and Eberhard Schlatter
Journal of Pharmacology and Experimental Therapeutics September 1, 2000, 294 (3) 1182-1187;

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Research ArticleCARDIOVASCULAR

Heterogenous Vascular Effects of AP5A in Different Rat Resistance Arteries Are Due to Heterogenous Distribution of P2X and P2Y1 Purinoceptors

Martin Steinmetz, Stefan Bierer, Peter Hollah, Karl Heinz Rahn and Eberhard Schlatter
Journal of Pharmacology and Experimental Therapeutics September 1, 2000, 294 (3) 1182-1187;
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