Involvement of N-methyl-d-aspartate glutamate receptor and nitric oxide in cardiovascular responses to dynamic exercise in rats

dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorCamargo, Laura H.A
dc.creatorAlves, Fernando H.F.
dc.creatorBiojone, Caroline
dc.creatorCorrea, Fernando M.A.
dc.creatorResstel, Leonardo B.M.
dc.creatorCrestani, Carlos Cesar
dc.date2014-05-27T11:29:38Z
dc.date2016-10-25T18:49:37Z
dc.date2014-05-27T11:29:38Z
dc.date2016-10-25T18:49:37Z
dc.date2013-06-03
dc.date.accessioned2017-04-06T02:26:07Z
dc.date.available2017-04-06T02:26:07Z
dc.identifierEuropean Journal of Pharmacology, v. 713, n. 1-3, p. 16-24, 2013.
dc.identifier0014-2999
dc.identifier1879-0712
dc.identifierhttp://hdl.handle.net/11449/75603
dc.identifierhttp://acervodigital.unesp.br/handle/11449/75603
dc.identifier10.1016/j.ejphar.2013.04.046
dc.identifierWOS:000320903900003
dc.identifier2-s2.0-84878253771.pdf
dc.identifier2-s2.0-84878253771
dc.identifierhttp://dx.doi.org/10.1016/j.ejphar.2013.04.046
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/896343
dc.descriptionDynamic 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.
dc.languageeng
dc.relationEuropean Journal of Pharmacology
dc.rightsinfo:eu-repo/semantics/openAccess
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 rats
dc.typeOtro


Este ítem pertenece a la siguiente institución