Publicação:
Cardiovascular responses to microinjection of L-glutamate into the NTS in AV3V-lesioned rats

dc.contributor.authorVieira, A. A.
dc.contributor.authorColombari, Eduardo [UNESP]
dc.contributor.authorDe Luca, L. A.
dc.contributor.authorColombari, DSD
dc.contributor.authorMenani, José Vanderlei [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2014-05-20T13:45:39Z
dc.date.available2014-05-20T13:45:39Z
dc.date.issued2004-10-29
dc.description.abstractThe excitatory amino acid L-glutamate injected into the nucleus of the solitary tract (NTS) in unanesthetized rats similar to peripheral chemoreceptor activation increases mean arterial pressure (MAP) and reduces heart rate. In this study, we investigated the effects of acute (I day) and chronic (15 days) electrolytic lesions of the preoptic-periventricular tissue surrounding the anteroventral third ventricle (AV3V region) on the pressor and bradycardic responses induced by injections of L-glutamate into the NTS or peripheral chemoreceptor activation in unanesthetized rats. Male Holtzman rats with sham or electrolytic AV3V lesions and a stainless steel cannula implanted into the NTS were used. Differently from the pressor responses (28 +/- 3 mm Hg) produced by injections into the NTS of sham-lesioned rats, L-glutamate (5 nmol/ 100 nl) injected into the NTS reduced MAP (-26 +/- 8 mm Hg) or produced no effect (2 7 turn Hg) in acute and chronic AV3V-lesioned rats, respectively. The bradycardia to L-glutamate into the NTS and the cardiovascular responses to chemoreflex activation with intravenous potassium cyanide or to baroreflex activation with intravenous phenylephrine or sodium nitroprusside were not modified by AV3V lesions. The results show that the integrity of the AV3V region is essential for the pressor responses to L-glutamate into the NTS but not for the pressor responses to chemoreflex activation, suggesting dissociation between the central mechanisms involved in these responses. (C) 2004 Elsevier B.V. All rights reserved.en
dc.description.affiliationUNESP, Dept Fisiol & Patol, Fac Odontol Araraquara, Sch Dent, BR-14801903 Araraquara, SP, Brazil
dc.description.affiliationUNIFESP, EPM, Dept Physiol, São Paulo, Brazil
dc.description.affiliationUnespUNESP, Dept Fisiol & Patol, Fac Odontol Araraquara, Sch Dent, BR-14801903 Araraquara, SP, Brazil
dc.format.extent106-112
dc.identifierhttp://dx.doi.org/10.1016/j.brainres.2004.08.006
dc.identifier.citationBrain Research. Amsterdam: Elsevier B.V., v. 1025, n. 1-2, p. 106-112, 2004.
dc.identifier.doi10.1016/j.brainres.2004.08.006
dc.identifier.issn0006-8993
dc.identifier.lattes4544450092427426
dc.identifier.lattes1023597870118105
dc.identifier.urihttp://hdl.handle.net/11449/16065
dc.identifier.wosWOS:000224682700013
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofBrain Research
dc.relation.ispartofjcr3.125
dc.relation.ispartofsjr1,404
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectbaroreceptorpt
dc.subjectchemoreceptorpt
dc.subjectsolitary tractpt
dc.subjecthypothalamuspt
dc.subjecthypertensionpt
dc.titleCardiovascular responses to microinjection of L-glutamate into the NTS in AV3V-lesioned ratsen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dspace.entity.typePublication
unesp.author.lattes4544450092427426[2]
unesp.author.lattes1023597870118105
unesp.author.orcid0000-0002-1395-4036[2]
unesp.author.orcid0000-0003-1167-4441[5]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquarapt
unesp.departmentFisiologia e Patologia - FOARpt

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