Alteration of Purinergic Neurotransmission in Isolated Atria of Streptozotocin-induced Diabetic Rats

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dc.contributor.authorMusial, Diego Castro [UNIFESP]
dc.contributor.authorGalvao, Kleber de Magalhaes [UNIFESP]
dc.contributor.authorMiranda-Ferreira, Regiane [UNIFESP]
dc.contributor.authorSilva Junior, Edilson Dantas da [UNIFESP]
dc.contributor.authorCaricati-Neto, Afonso [UNIFESP]
dc.contributor.authorJurkiewicz, Neide Hyppolito [UNIFESP]
dc.contributor.authorJurkiewicz, Aron [UNIFESP]
dc.contributor.authorBroetto Biazon, Ana Carla
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T14:17:53Z
dc.date.available2016-01-24T14:17:53Z
dc.date.issued2012-02-01
dc.description.abstractCardiac dysfunctions are described in diabetes. However, the role of purinergic neurotransmission in diabetes-related cardiovascular diseases is unknown. the purpose of this study was to evaluate the purinergic neurotransmission in isolated atria from streptozotocin-induced diabetic rats. the animals were grouped as control and diabetic with 30 days (D30) and 60 days (D60) after streptozotocin-induced diabetes. the isolated left and right atria were used in functional experiments. the effects of adenosine triphosphate, uridine diphosphate, and adenosine were evaluated on atrial inotropism and chronotropism. the antagonists 8-cyclopentyl-1,3-dipropylxanthine and pyridoxal-phosphate-6-azophenyl-2', 4'-disulfonate were also used, as blockers of P-1 and P-2 receptors, respectively. A negative inotropic effect followed by a positive inotropic effect was induced by adenosine triphosphate in isolated atria. This negative inotropic effect was decreased by 25% in left atria of D30. Additionally, the apparent affinity for adenosine was diminished in left atria of D30, suggesting changes in P1 receptor function. No changes were found in the right atria of D30 stimulated by adenosine. the left atria and right atria stimulated by uridine diphosphate showed an increased inotropic effect of 92% and 17%, respectively. No changes were observed in left and right atria of D30 stimulated by uridine diphosphate. Our data showed the involvement of purinergic neurotransmission in diabetes-related cardiovascular changes.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Pharmacol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Pharmacol, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent158-164
dc.identifierhttp://dx.doi.org/10.1097/FJC.0b013e31823a0f31
dc.identifier.citationJournal of Cardiovascular Pharmacology. Philadelphia: Lippincott Williams & Wilkins, v. 59, n. 2, p. 158-164, 2012.
dc.identifier.doi10.1097/FJC.0b013e31823a0f31
dc.identifier.issn0160-2446
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/34602
dc.identifier.wosWOS:000300403000007
dc.language.isoeng
dc.publisherLippincott Williams & Wilkins
dc.relation.ispartofJournal of Cardiovascular Pharmacology
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectisolated atriaen
dc.subjectpurinergic neurotransmissionen
dc.subjectpurinergic receptorsen
dc.subjectstreptozotocin-induced diabetic ratsen
dc.titleAlteration of Purinergic Neurotransmission in Isolated Atria of Streptozotocin-induced Diabetic Ratsen
dc.typeinfo:eu-repo/semantics/article
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