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dc.contributor.authorGe, Zhi-Dongen_US
dc.contributor.authorN. Peart, Jasonen_US
dc.contributor.authorM. Kreckler, Lauraen_US
dc.contributor.authorC. Wan, Tinaen_US
dc.contributor.authorA. Jacobson, Marleneen_US
dc.contributor.authorJ. Gross, Garretten_US
dc.contributor.authorA. Auchampach, Johnen_US
dc.date.accessioned2017-05-03T13:03:40Z
dc.date.available2017-05-03T13:03:40Z
dc.date.issued2006en_US
dc.date.modified2009-12-22T03:07:28Z
dc.identifier.issn00223565en_US
dc.identifier.doi10.1124/jpet.106.111351en_AU
dc.identifier.urihttp://hdl.handle.net/10072/27908
dc.description.abstractWe used pharmacological agents and genetic methods to determine whether the potent A3 adenosine receptor (AR) agonist 2-chloro-N6-(3-iodobenzyl)adenosine-5 -N-methylcarboxamide (Cl-IB-MECA) protects against myocardial ischemia/ reperfusion injury in mice via the A3AR or via interactions with other AR subtypes. Pretreating wild-type (WT) mice with Cl-IBMECA reduced myocardial infarct size induced by 30 min of coronary occlusion and 24 h of reperfusion at doses (30 and 100 姯kg) that concomitantly reduced blood pressure and stimulated systemic histamine release. The A3AR-selective antagonist MRS 1523 [3-propyl-6-ethyl-5[(ethylthio)carbonyl]-2-phenyl-4-propyl-3-pyridine-carboxylate], but not the A2AAR antagonist ZM 241385 [4-{2-7-amino-2-(2-furyl)[1,2,4]triazolo-[2,3-a][1,3,5]triazin-5-ylamino]ethyl}phenol], blocked the reduction in infarct size provided by Cl-IB-MECA, suggesting a mechanism involving the A3AR. To further examine the selectivity of Cl-IB-MECA, we assessed its cardioprotective effectiveness in A3AR gene "knock-out" (A3KO) mice. Cl-IB-MECA did not reduce myocardial infarct size in A3KO mice in vivo and did not protect isolated perfused hearts obtained from A3KO mice from injury induced by global ischemia and reperfusion. Additional studies using WT mice treated with compound 48/80 [condensation product of ?-methoxyphenethyl methylamine with formaldehyde] to deplete mast cell contents excluded the possibility that Cl-IB-MECA was cardioprotective by releasing mediators from mast cells. These data demonstrate that Cl-IBMECA protects against myocardial ischemia/reperfusion injury in mice principally by activating the A3AR.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherThe American Society for Pharmacology and Experimental Therapeuticsen_US
dc.publisher.placeBaltimoreen_US
dc.publisher.urihttp://jpet.aspetjournals.org/en_AU
dc.relation.ispartofstudentpublicationNen_AU
dc.relation.ispartofpagefrom1200en_US
dc.relation.ispartofpageto1210en_US
dc.relation.ispartofissue3en_US
dc.relation.ispartofjournalJournal of Pharmacology and Experimental Therapeuticsen_US
dc.relation.ispartofvolume319en_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchcode320503en_US
dc.titleCl-IB-MECA [2-Chloro-N6-(3-iodobenzyl)adenosine-5'-N-methylcarboxamide] Reduces Ischemia/Reperfusion Injury in Mice by Activating the A Adenosine Receptoren_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.date.issued2006
gro.hasfulltextNo Full Text


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