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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<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Kalkan, S.</dc:creator>
  <dc:creator>Oransay, K.</dc:creator>
  <dc:creator>Bal, I. B.</dc:creator>
  <dc:creator>Ertunc, M.</dc:creator>
  <dc:creator>Sara, Y.</dc:creator>
  <dc:creator>Iskit, A. B.</dc:creator>
  <dc:date>2013-01-01</dc:date>
  <dc: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 &lt; 0.001) and the maximum rise slope of AP was reduced by amitriptyline (p &lt; 0.0001). Amitriptyline reduced maximum decay slope of AP only at 50 mu M (p &lt; 0.01). DPCPX significantly decreased the 50-mu M amitriptyline-induced APD(50) and APD(80) prolongation (p &lt; 0.001). DPCPX significantly prevented the effects of amitriptyline (1 mu M and 50 mu M) on maximum rise slope of AP (p &lt; 0.05). DPCPX significantly prevented the amitriptyline-induced (50 mu M) reduction in maximum decay slope of AP (p &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.</dc:description>
  <dc:identifier>https://aperta.ulakbim.gov.trrecord/12335</dc:identifier>
  <dc:identifier>oai:zenodo.org:12335</dc:identifier>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights>
  <dc:source>HUMAN &amp; EXPERIMENTAL TOXICOLOGY 32(1) 62-69</dc:source>
  <dc:title>The role of adenosine receptors on amitriptyline-induced electrophysiological changes on rat atrium</dc:title>
  <dc:type>info:eu-repo/semantics/article</dc:type>
  <dc:type>publication-article</dc:type>
</oai_dc:dc>