Cardiac arrest induced by muscarinic or adenosine receptors agonists is reversed by DPCPX through double mechanism

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dc.citation.volume819
dc.contributor.authorCamara, Henrique [UNIFESP]
dc.contributor.authorda Silva Junior, Edilson Dantas [UNIFESP]
dc.contributor.authorGarcia, Antonio G.
dc.contributor.authorJurkiewicz, Aron [UNIFESP]
dc.contributor.authorDantas Rodrigues, Juliano Quintella [UNIFESP]
dc.coverageAmsterdam
dc.date.accessioned2020-07-08T13:09:52Z
dc.date.available2020-07-08T13:09:52Z
dc.date.issued2018
dc.description.abstractIn the right atrium (RA), adenosine and acetylcholine inhibit the pacemaker function of the sinoatrial node and induce cardiac arrest. Pre-incubation of receptor antagonists is known to inhibit the cardiac arrest induced by these agonistsen
dc.description.abstracthowever, the effect of antagonist administration after established cardiac arrest has not been described. Therefore, we assessed whether specific receptor antagonists could revert cardiac arrest induced by adenosine and muscarinic receptors activation. RA isolated from adults Wistar rats were mounted in an organ bath containing Krebs solution. Cardiac arrest was induced by adenosine or ATP (1 mM), the A(1) adenosine receptor agonist CPA (0.1-1 mu M), and muscarinic receptor agonists, carbachol (0.3-1 mu M) and acetylcholine (1 mM). After establishing the cardiac arrest, the A1 adenosine receptor antagonist DPCPX (0.3-30 mu M), the muscarinic receptor antagonist atropine (10 nM to 100 mu M) or the phosphodiesterase inhibitor IBMX (10-300 mu M) were incubated in order to check for the return of spontaneous contractions. DPCPX reversed the cardiac arrest induced by adenosine, ATP and CPA. In addition, atropine reversed the cardiac arrest induced by carbachol. Unexpectedly, DPCPX also reversed the cardiac arrest induced by carbachol. Similarly to DPCPX, the phosphodiesterase inhibitor IBMX reversed the cardiac arrest induced by adenosine, CPA and carbachol. The antagonism of adenosine and acetylcholine receptors activation, as well as phosphodiesterase inhibition, are able to revert cardiac arrest. DPCPX restore spontaneous contractions via the selective antagonism of A1 adenosine receptor and through a secondary mechanism likely related to phosphodiesterase inhibition.en
dc.description.affiliationFed Univ Sao Paulo UNIFESP, Dept Pharmacol, Sao Paulo, Brazil
dc.description.affiliationUniv Autonoma Madrid, Inst Teofilo Hernando, Madrid, Spain
dc.description.affiliationUnifespFed Univ Sao Paulo UNIFESP, Dept Pharmacol, Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFAPESP
dc.description.sponsorshipCapes
dc.description.sponsorshipIDFAPESP: 13/20402-6
dc.description.sponsorshipIDCapes: PNPD - 1864/2008
dc.format.extentset/15
dc.identifierhttp://dx.doi.org/10.1016/j.ejphar.2017.09.030
dc.identifier.citationEuropean Journal Of Pharmacology. Amsterdam, v. 819, p. 42248, 2018.
dc.identifier.doi10.1016/j.ejphar.2017.09.030
dc.identifier.issn0014-2999
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/54263
dc.identifier.wosWOS:000419629200002
dc.language.isoeng
dc.publisherElsevier Science Bv
dc.relation.ispartofEuropean Journal Of Pharmacology
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectCardiac arresten
dc.subjectSinoatrial nodeen
dc.subjectAdenosine receptoren
dc.subjectMuscarinic receptoren
dc.subjectDPCPXen
dc.titleCardiac arrest induced by muscarinic or adenosine receptors agonists is reversed by DPCPX through double mechanismen
dc.typeinfo:eu-repo/semantics/article
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