1 Ocak 2013 Dergi makalesi Açık Erişim

Kalkan, S.; Oransay, K.; Bal, I. B.; Ertunc, M.; Sara, Y.; Iskit, A. B.

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        "affiliation": "Dokuz Eylul Univ, Dept Pharmacol, Sch Med, TR-35340 Izmir, Turkey", 
        "name": "Kalkan, S."
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      {
        "affiliation": "Dokuz Eylul Univ, Dept Pharmacol, Sch Med, TR-35340 Izmir, Turkey", 
        "name": "Oransay, K."
      }, 
      {
        "affiliation": "Hacettepe Univ, Dept Pharmacol, Fac Med, Ankara, Turkey", 
        "name": "Bal, I. B."
      }, 
      {
        "affiliation": "Hacettepe Univ, Dept Pharmacol, Fac Med, Ankara, Turkey", 
        "name": "Ertunc, M."
      }, 
      {
        "affiliation": "Hacettepe Univ, Dept Pharmacol, Fac Med, Ankara, Turkey", 
        "name": "Sara, Y."
      }, 
      {
        "affiliation": "Hacettepe Univ, Dept Pharmacol, Fac Med, Ankara, Turkey", 
        "name": "Iskit, A. B."
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    "description": "We investigated the role of adenosine receptors in amitriptyline-induced cardiac action potential (AP) changes in isolated rat atria. In the first group, APs were recorded after cumulative addition of amitriptyline (1 mu M, 10 mu M and 50 mu M). In other groups, each atrium was incubated with selective adenosine A(1) antagonist (8-cyclopentyl-1,3-dipropylxanthine (DPCPX), 10(-4) M) or selective adenosine A(2a) receptor antagonist (8-(3-chlorostyryl) caffeine, 10(-5) M) before amitriptyline administration. Resting membrane potential, AP amplitude (APA), AP duration at 50% and 80% of repolarization (APD(50) and APD(80), respectively), and the maximum rise and decay slopes of AP were recorded. Amitriptyline (50 mu M) prolonged the APD(50) and APD(80) (p < 0.001) and the maximum rise slope of AP was reduced by amitriptyline (p < 0.0001). Amitriptyline reduced maximum decay slope of AP only at 50 mu M (p < 0.01). DPCPX significantly decreased the 50-mu M amitriptyline-induced APD(50) and APD(80) prolongation (p < 0.001). DPCPX significantly prevented the effects of amitriptyline (1 mu M and 50 mu M) on maximum rise slope of AP (p < 0.05). DPCPX significantly prevented the amitriptyline-induced (50 mu M) reduction in maximum decay slope of AP (p < 0.001). The selective adenosine A(1) receptor antagonist prevented the electrophysiological effects of amitriptyline on atrial AP. A(1) receptor stimulation may be responsible for the cardiovascular toxic effects produced by amitriptyline.", 
    "doi": "10.1177/0960327112455670", 
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    "journal": {
      "issue": "1", 
      "pages": "62-69", 
      "title": "HUMAN & EXPERIMENTAL TOXICOLOGY", 
      "volume": "32"
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    "publication_date": "2013-01-01", 
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    "resource_type": {
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      "title": "Dergi makalesi", 
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    "title": "The role of adenosine receptors on amitriptyline-induced electrophysiological changes on rat atrium"
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