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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    <subfield code="a">The role of adenosine receptors on amitriptyline-induced electrophysiological changes on rat atrium</subfield>
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    <subfield code="a">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 &amp;lt; 0.001) and the maximum rise slope of AP was reduced by amitriptyline (p &amp;lt; 0.0001). Amitriptyline reduced maximum decay slope of AP only at 50 mu M (p &amp;lt; 0.01). DPCPX significantly decreased the 50-mu M amitriptyline-induced APD(50) and APD(80) prolongation (p &amp;lt; 0.001). DPCPX significantly prevented the effects of amitriptyline (1 mu M and 50 mu M) on maximum rise slope of AP (p &amp;lt; 0.05). DPCPX significantly prevented the amitriptyline-induced (50 mu M) reduction in maximum decay slope of AP (p &amp;lt; 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.</subfield>
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    <subfield code="u">Dokuz Eylul Univ, Dept Pharmacol, Sch Med, TR-35340 Izmir, Turkey</subfield>
    <subfield code="a">Oransay, K.</subfield>
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    <subfield code="u">Hacettepe Univ, Dept Pharmacol, Fac Med, Ankara, Turkey</subfield>
    <subfield code="a">Bal, I. B.</subfield>
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    <subfield code="a">Ertunc, M.</subfield>
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    <subfield code="a">Iskit, A. B.</subfield>
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    <subfield code="u">Dokuz Eylul Univ, Dept Pharmacol, Sch Med, TR-35340 Izmir, Turkey</subfield>
    <subfield code="a">Kalkan, S.</subfield>
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