1 Ocak 2013 Dergi makalesi Açık Erişim

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

DataCite XML

<?xml version='1.0' encoding='utf-8'?>
<resource xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns="http://datacite.org/schema/kernel-4" xsi:schemaLocation="http://datacite.org/schema/kernel-4 http://schema.datacite.org/meta/kernel-4.1/metadata.xsd">
  <identifier identifierType="URL">https://aperta.ulakbim.gov.tr/record/12335</identifier>
  <creators>
    <creator>
      <creatorName>Kalkan, S.</creatorName>
      <givenName>S.</givenName>
      <familyName>Kalkan</familyName>
      <affiliation>Dokuz Eylul Univ, Dept Pharmacol, Sch Med, TR-35340 Izmir, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Oransay, K.</creatorName>
      <givenName>K.</givenName>
      <familyName>Oransay</familyName>
      <affiliation>Dokuz Eylul Univ, Dept Pharmacol, Sch Med, TR-35340 Izmir, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Bal, I. B.</creatorName>
      <givenName>I. B.</givenName>
      <familyName>Bal</familyName>
      <affiliation>Hacettepe Univ, Dept Pharmacol, Fac Med, Ankara, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Ertunc, M.</creatorName>
      <givenName>M.</givenName>
      <familyName>Ertunc</familyName>
      <affiliation>Hacettepe Univ, Dept Pharmacol, Fac Med, Ankara, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Sara, Y.</creatorName>
      <givenName>Y.</givenName>
      <familyName>Sara</familyName>
      <affiliation>Hacettepe Univ, Dept Pharmacol, Fac Med, Ankara, Turkey</affiliation>
    </creator>
    <creator>
      <creatorName>Iskit, A. B.</creatorName>
      <givenName>A. B.</givenName>
      <familyName>Iskit</familyName>
      <affiliation>Hacettepe Univ, Dept Pharmacol, Fac Med, Ankara, Turkey</affiliation>
    </creator>
  </creators>
  <titles>
    <title>The Role Of Adenosine Receptors On Amitriptyline-Induced Electrophysiological Changes On Rat Atrium</title>
  </titles>
  <publisher>Aperta</publisher>
  <publicationYear>2013</publicationYear>
  <dates>
    <date dateType="Issued">2013-01-01</date>
  </dates>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
  <alternateIdentifiers>
    <alternateIdentifier alternateIdentifierType="url">https://aperta.ulakbim.gov.tr/record/12335</alternateIdentifier>
  </alternateIdentifiers>
  <relatedIdentifiers>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1177/0960327112455670</relatedIdentifier>
  </relatedIdentifiers>
  <rightsList>
    <rights rightsURI="http://www.opendefinition.org/licenses/cc-by">Creative Commons Attribution</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
  </rightsList>
  <descriptions>
    <description descriptionType="Abstract">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.</description>
  </descriptions>
</resource>