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AV3V LESION REDUCES THE PRESSOR, DIPSOGENIC, AND NATRIURETIC RESPONSES TO VENTROMEDIAL HYPOTHALAMUS ACTIVATION

dc.contributor.authorValladao, A. S.
dc.contributor.authorSaad, W. A.
dc.contributor.authorCamargo, LAD
dc.contributor.authorRenzi, Antonio [UNESP]
dc.contributor.authorDeluca, L. A.
dc.contributor.authorMenani, José Vanderlei [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T15:28:17Z
dc.date.available2014-05-20T15:28:17Z
dc.date.issued1992-06-01
dc.description.abstractIn the present study, we investigated the effect of anteroventral third ventricle (AV3V) lesion on pressor, tachycardic, dipsogenic, natriuretic, and kaliuretic responses induced by the injection of the cholinergic agonist carbachol into the ventromedial hypothalamic nucleus (VMH) of rats. Male rats with sham or AV3V lesion and a stainless steel cannula implanted into the VMH were used. Carbachol (2 nmol) injected into the VMH of sham rats produced pressor (32 +/- 4 mmHg). tachycardic (83 +/- 14 bpm), dipsogenic (8.2 +/- 1.1 ml/h). natriuretic (320 +/- 46-mu-Eq/120 min), and kaliuretic (155 +/- 20-mu-Eq/120 min) responses. In AV3V-lesioned rats (2 and 15 days), the pressor (4 +/- 2 and 15 +/- 2 mmHg. respectively), dipsogenic (0.3 +/-0.2 and 1.4 +/- 0.7 ml/h), natriuretic (17 +/- 7 and 99 +/- 21-mu-Eq/120 min), and kaliuretic (76 +/- 14 and 79 +/- 7-mu-Eq/120 min) responses induced by carbachol injection into the VMH were reduced. The tachycardia was also abolished (27 +/- 15 and -23 +/-29 bpm, respectively). These results show that the AV3V region is essential for the pressor, tachycardic, dipsogenic, natriuretic. and kaliuretic responses induced hy cholinergic activation of the VMH in rats.en
dc.description.affiliationPAULISTA STATE UNIV,SCH DENT,DEPT PHYSIOL,1680 HUMAITA ST,BR-14800 ARARAQUARA,SP,BRAZIL
dc.description.affiliationUnespPAULISTA STATE UNIV,SCH DENT,DEPT PHYSIOL,1680 HUMAITA ST,BR-14800 ARARAQUARA,SP,BRAZIL
dc.format.extent909-914
dc.identifierhttp://dx.doi.org/10.1016/0361-9230(92)90211-F
dc.identifier.citationBrain Research Bulletin. Oxford: Pergamon-Elsevier B.V., v. 28, n. 6, p. 909-914, 1992.
dc.identifier.doi10.1016/0361-9230(92)90211-F
dc.identifier.issn0361-9230
dc.identifier.lattes6551236936295697
dc.identifier.lattes1023597870118105
dc.identifier.urihttp://hdl.handle.net/11449/38111
dc.identifier.wosWOS:A1992JA27200009
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofBrain Research Bulletin
dc.relation.ispartofjcr3.440
dc.relation.ispartofsjr1,398
dc.rights.accessRightsAcesso restritopt
dc.sourceWeb of Science
dc.subjectARTERIAL PRESSUREpt
dc.subjectWATER INTAKEpt
dc.subjectFLUID BALANCEpt
dc.subjectELECTROLYTE BALANCEpt
dc.subjectAV3V REGIONpt
dc.titleAV3V LESION REDUCES THE PRESSOR, DIPSOGENIC, AND NATRIURETIC RESPONSES TO VENTROMEDIAL HYPOTHALAMUS ACTIVATIONen
dc.typeArtigopt
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dspace.entity.typePublication
relation.isDepartmentOfPublicationb3ba3d9c-022e-4521-8805-0bcceea7372e
relation.isDepartmentOfPublication.latestForDiscoveryb3ba3d9c-022e-4521-8805-0bcceea7372e
relation.isOrgUnitOfPublicationca4c0298-cd82-48ee-a9c8-c97704bac2b0
relation.isOrgUnitOfPublication.latestForDiscoveryca4c0298-cd82-48ee-a9c8-c97704bac2b0
unesp.author.lattes6551236936295697
unesp.author.lattes1023597870118105
unesp.author.orcid0000-0003-1167-4441[6]
unesp.author.orcid0000-0001-8270-2652[5]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquarapt
unesp.departmentFisiologia e Patologia - FOARpt

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