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    Adenosine A1 receptor-mediated antiadrenergic effects are modulated by A2a receptor activation in rat heart

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    Authors
    Norton, Gavin R.
    Woodiwiss, Angela J.
    McGinn, Robert J.
    Lorbar, Mojca
    Chung, Eugene S.
    Honeyman, Thomas W.
    Fenton, Richard A.
    Dobson, James G.
    Meyer, Theo E.
    UMass Chan Affiliations
    Department of Physiology
    Document Type
    Journal Article
    Publication Date
    1999-02-10
    Keywords
    Adenosine
    Adrenergic alpha-Antagonists
    Animals
    Calcium
    Drug Synergism
    Heart
    Intracellular Membranes
    Male
    Myocardium
    Osmolar Concentration
    Rats
    Rats, Sprague-Dawley
    Receptors, Purinergic P1
    Triazines
    Triazoles
    Physiology
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    Link to Full Text
    http://ajpheart.physiology.org/cgi/content/full/276/2/H341
    Abstract
    Presently, the physiological significance of myocardial adenosine A2a receptor stimulation is unclear. In this study, the influence of adenosine A2a receptor activation on A1 receptor-mediated antiadrenergic actions was studied using constant-flow perfused rat hearts and isolated rat ventricular myocytes. In isolated perfused hearts, the selective A2a receptor antagonists 8-(3-chlorostyryl)caffeine (CSC) and 4-(2-[7-amino-2-(2-furyl)[1,2, 4]triazolo[2,3-a][1,3,5]triazin-5-ylamino]ethyl)phenol (ZM-241385) potentiated adenosine-mediated decreases in isoproterenol (Iso; 10(-8) M)-elicited contractile responses (+dP/dtmax) in a dose-dependent manner. The effect of ZM-241385 on adenosine-induced antiadrenergic actions was abolished by the selective A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (10(-7) M), but not the selective A3 receptor antagonist 3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1, 4-(+/-)-dihydropyridine-3,5-dicarboxylate (MRS-1191, 10(-7) M). The A2a receptor agonist carboxyethylphenethyl-aminoethyl-carboxyamido-adenosine (CGS-21680) at 10(-5) M attenuated the antiadrenergic effect of the selective A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA), whereas CSC did not influence the antiadrenergic action of this agonist. In isolated ventricular myocytes, CSC potentiated the inhibitory action of adenosine on Iso (2 x 10(-7) M)-elicited increases in intracellular Ca2+ concentration ([Ca2+]i) transients but did not influence Iso-induced changes in [Ca2+]i transients in the absence of exogenous adenosine. These results indicate that adenosine A2a receptor antagonists enhance A1-receptor-induced antiadrenergic responses and that A2a receptor agonists attenuate (albeit to a modest degree) the antiadrenergic actions of A1 receptor activation. In conclusion, the data in this study support the notion that an important physiological role of A2a receptors in the normal mammalian myocardium is to reduce A1 receptor-mediated antiadrenergic actions.
    Source
    Am J Physiol. 1999 Feb;276(2 Pt 2):H341-9.
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/44134
    PubMed ID
    9950832
    Related Resources
    Link to article in PubMed
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    UMass Chan Faculty and Researcher Publications

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