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Please use this identifier to cite or link to this item: http://acervodigital.unesp.br/handle/11449/75603
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dc.contributor.authorCamargo, Laura H.A-
dc.contributor.authorAlves, Fernando H.F.-
dc.contributor.authorBiojone, Caroline-
dc.contributor.authorCorrea, Fernando M.A.-
dc.contributor.authorResstel, Leonardo B.M.-
dc.contributor.authorCrestani, Carlos Cesar-
dc.date.accessioned2014-05-27T11:29:38Z-
dc.date.accessioned2016-10-25T18:49:37Z-
dc.date.available2014-05-27T11:29:38Z-
dc.date.available2016-10-25T18:49:37Z-
dc.date.issued2013-06-03-
dc.identifierhttp://dx.doi.org/10.1016/j.ejphar.2013.04.046-
dc.identifier.citationEuropean Journal of Pharmacology, v. 713, n. 1-3, p. 16-24, 2013.-
dc.identifier.issn0014-2999-
dc.identifier.issn1879-0712-
dc.identifier.urihttp://hdl.handle.net/11449/75603-
dc.identifier.urihttp://acervodigital.unesp.br/handle/11449/75603-
dc.description.abstractDynamic exercise evokes sustained cardiovascular responses, which are characterized by arterial pressure and heart rate increases. Although it is well accepted that there is central nervous system mediation of cardiovascular adjustments during exercise, information on the role of neural pathways and signaling mechanisms is limited. It has been reported that glutamate, by acting on NMDA receptors, evokes the release of nitric oxide through activation of neuronal nitric oxide synthase (nNOS) in the brain. In the present study, we tested the hypothesis that NMDA receptors and nNOS are involved in cardiovascular responses evoked by an acute bout of exercise on a rodent treadmill. Moreover, we investigated possible central sites mediating control of responses to exercise through the NMDA receptor-nitric oxide pathway. Intraperitoneal administration of the selective NMDA glutamate receptor antagonist dizocilpine maleate (MK-801) reduced both the arterial pressure and heart rate increase evoked by dynamic exercise. Intraperitoneal treatment with the preferential nNOS inhibitor 7-nitroindazole reduced exercise-evoked tachycardiac response without affecting the pressor response. Moreover, treadmill running increased NO formation in the medial prefrontal cortex (MPFC), bed nucleus of the stria teminalis (BNST) and periaqueductal gray (PAG), and this effect was inhibited by systemic pretreatment with MK-801. Our findings demonstrate that NMDA receptors and nNOS mediate the tachycardiac response to dynamic exercise, possibly through an NMDA receptor-NO signaling mechanism. However, NMDA receptors, but not nNOS, mediate the exercise-evoked pressor response. The present results also provide evidence that MPFC, BNST and PAG may modulate physiological adjustments during dynamic exercise through NMDA receptor-NO signaling. © 2013 Elsevier B.V.en
dc.format.extent16-24-
dc.language.isoeng-
dc.sourceScopus-
dc.subjectBNST-
dc.subjectExercise-
dc.subjectGlutamate-
dc.subjectHippocampus-
dc.subjectMPFC-
dc.subjectNeuronal nitric oxide-
dc.subjectPAG-
dc.subjectPVN-
dc.subjectsynthase-
dc.subject7 nitroindazole-
dc.subjectdizocilpine-
dc.subjectn methyl dextro aspartic acid receptor-
dc.subjectnitric oxide synthase-
dc.subjectanimal experiment-
dc.subjectanimal tissue-
dc.subjectarterial pressure-
dc.subjectcardiovascular response-
dc.subjectcontrolled study-
dc.subjectdynamic exercise-
dc.subjectenzyme activation-
dc.subjectheart rate-
dc.subjecthippocampus-
dc.subjectmale-
dc.subjectnonhuman-
dc.subjectparaventricular thalamic nucleus-
dc.subjectperiaqueductal gray matter-
dc.subjectprefrontal cortex-
dc.subjectpriority journal-
dc.subjectprotein synthesis-
dc.subjectrat-
dc.subjectsignal transduction-
dc.subjectstria terminalis-
dc.subjecttachycardia-
dc.subjecttreadmill exercise-
dc.titleInvolvement of N-methyl-d-aspartate glutamate receptor and nitric oxide in cardiovascular responses to dynamic exercise in ratsen
dc.typeoutro-
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)-
dc.contributor.institutionUniversidade de São Paulo (USP)-
dc.description.affiliationDepartment of Natural Active Principles and Toxicology School of Pharmaceutical Sciences São Paulo State University, Rodovia Araraquara-Jau Km 01, Caixa Postal 502, Araraquara, SP, 14801-902-
dc.description.affiliationDepartment of Pharmacology School of Medicine of Ribeirão Preto University of São Paulo, Ribeirão Preto, SP, 14049-900-
dc.description.affiliationUnespDepartment of Natural Active Principles and Toxicology School of Pharmaceutical Sciences São Paulo State University, Rodovia Araraquara-Jau Km 01, Caixa Postal 502, Araraquara, SP, 14801-902-
dc.identifier.doi10.1016/j.ejphar.2013.04.046-
dc.identifier.wosWOS:000320903900003-
dc.rights.accessRightsAcesso aberto-
dc.identifier.file2-s2.0-84878253771.pdf-
dc.relation.ispartofEuropean Journal of Pharmacology-
dc.identifier.scopus2-s2.0-84878253771-
Appears in Collections:Artigos, TCCs, Teses e Dissertações da Unesp

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