Ventromedial hypothalamus lesions increase the dipsogenic responses and reduce the pressor responses to median preoptic area activation

dc.contributor.authorBastos, R.
dc.contributor.authorMenani, José Vanderlei [UNESP]
dc.contributor.authorSaad, W. A.
dc.contributor.authorRenzi, Antonio [UNESP]
dc.contributor.authorSilveira, JEN
dc.contributor.authorCamargo, LADA
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T15:25:10Z
dc.date.available2014-05-20T15:25:10Z
dc.date.issued1997-08-01
dc.description.abstractIn this study, we investigated the participation of adrenergic receptors of the median preoptic area (MnPO) and the participation of ventromedial hypothalamus (VMH) in angiotensin II- (ANG II)-induced water intake and presser responses. Male rats with sham or electrolytic VMH lesions and a stainless steel cannula implanted into the MnPO were used. Noradrenaline, clonidine (an alpha(2)-adrenergic receptor agonist), or phenylephrine (an alpha(1)-adrenergic receptor agonist) injected into the MnPO of sham-lesioned rats reduced water ingestion induced by ANG II injected into the same area. In VMH-lesioned rats ANG II-induced water intake increased with a previous injection of noradrenaline, phenylephrine, or isoproterenol. The presser response induced by ANG II injected into the MnPO was reduced in VMH-lesioned rats, whereas the presser response induced by clonidine was abolished. Previous treatment with noradrenaline and phenylephrine into the MnPO of sham-lesioned rats produced a presser response, and a hypotensive response was obtained with the previous administration of noradrenaline, phenylephrine or isoproterenol into the MnPO of VMH-lesioned rats. These results show that VMH is essential for the dipsogenic and presser responses induced by adrenergic and angiotensinergic activation of the MnPO in rats. (C) 1997 Elsevier B.V.en
dc.description.affiliationPAULISTA STATE UNIV,UNESP,SCH DENT,DEPT PHYSIOL,BR-14801903 ARARAQUARA,SP,BRAZIL
dc.description.affiliationUnespPAULISTA STATE UNIV,UNESP,SCH DENT,DEPT PHYSIOL,BR-14801903 ARARAQUARA,SP,BRAZIL
dc.format.extent311-316
dc.identifierhttp://dx.doi.org/10.1016/S0031-9384(97)88986-X
dc.identifier.citationPhysiology & Behavior. Oxford: Pergamon-Elsevier B.V., v. 62, n. 2, p. 311-316, 1997.
dc.identifier.doi10.1016/S0031-9384(97)88986-X
dc.identifier.issn0031-9384
dc.identifier.lattes1023597870118105
dc.identifier.lattes6551236936295697
dc.identifier.urihttp://hdl.handle.net/11449/35627
dc.identifier.wosWOS:A1997XN41000013
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofPhysiology & Behavior
dc.relation.ispartofjcr2.517
dc.relation.ispartofsjr1,088
dc.rights.accessRightsAcesso restrito
dc.sourceWeb of Science
dc.subjectwater intakept
dc.subjectarterial pressurept
dc.subjectANG IIpt
dc.subjectadrenergic agonistspt
dc.subjectMnPOpt
dc.subjectVMHpt
dc.titleVentromedial hypothalamus lesions increase the dipsogenic responses and reduce the pressor responses to median preoptic area activationen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
unesp.author.lattes1023597870118105
unesp.author.lattes6551236936295697
unesp.author.orcid0000-0003-1167-4441[2]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araraquarapt

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