Rapid stimulation of sodium intake combining aldosterone into the 4th ventricle and the blockade of the lateral parabrachial nucleus

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dc.contributor.authorGasparini, S. [UNESP]
dc.contributor.authorMelo, M. R. [UNESP]
dc.contributor.authorLeite, G. F. [UNESP]
dc.contributor.authorNascimento, P. A. [UNESP]
dc.contributor.authorAndrade-Franzé, G. M.F. [UNESP]
dc.contributor.authorMenani, J. V. [UNESP]
dc.contributor.authorColombari, E. [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2018-12-11T17:09:50Z
dc.date.available2018-12-11T17:09:50Z
dc.date.issued2017-03-27
dc.description.abstractChronic infusion of aldosterone into the 4th ventricle (4th V) induces robust daily sodium intake, whereas acute injection of aldosterone into the 4th V produces no sodium intake. The inhibitory mechanism of the lateral parabrachial nucleus (LPBN) restrains sodium intake induced by different natriorexigenic stimuli and might affect the acute response to aldosterone into the 4th V. In the present study, 1.8% NaCl and water intake was tested in rats treated with acute injections of aldosterone into the 4th V combined with the blockade of the inhibitory mechanisms with injections of moxonidine (α2 adrenergic/imidazoline agonist) or methysergide (a serotonergic antagonist) into the LPBN. Male Holtzman rats with stainless steel cannulas implanted in the 4th V and bilaterally in the LPBN were used. Aldosterone (250 or 500 ng) into the 4th V combined with vehicle into the LPBN induced no 1.8% NaClintake compared to control (1.5 ± 1.1 and 1.1 ± 0.4, respectively, vs. vehicle into 4th V: 1.0 ± 0.5 ml/2 h). However, aldosterone (250 or 500 ng) into the 4th V combined with moxonidine (0.5 nmol) into the LPBN induced strong ingestion of 1.8% NaCl (12.7 ± 4.6 and 17.6 ± 3.7 ml/2 h, respectively). Aldosterone (250 ng) into the 4th V combined with methysergide (4 μg) into the LPBN also induced 1.8% NaCl intake (17.6 ± 5.4 ml/2 h). These data suggest that the inhibitory mechanisms of the LPBN counteract the facilitation of sodium intake produced by aldosterone injected into the 4th, restraining sodium intake in this condition.en
dc.description.affiliationDepartment of Physiology and Pathology School of Dentistry of Araraquara São Paulo State University UNESP
dc.description.affiliationUnespDepartment of Physiology and Pathology School of Dentistry of Araraquara São Paulo State University UNESP
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipIdFAPESP: 2015/23467-7
dc.description.sponsorshipIdFAPESP: FAPESP 2011/50770-1
dc.description.sponsorshipIdFAPESP: FAPESP 2013/00026-0
dc.format.extent94-101
dc.identifierhttp://dx.doi.org/10.1016/j.neuroscience.2017.01.005
dc.identifier.citationNeuroscience, v. 346, p. 94-101.
dc.identifier.doi10.1016/j.neuroscience.2017.01.005
dc.identifier.file2-s2.0-85012272809.pdf
dc.identifier.issn1873-7544
dc.identifier.issn0306-4522
dc.identifier.scopus2-s2.0-85012272809
dc.identifier.urihttp://hdl.handle.net/11449/174204
dc.language.isoeng
dc.relation.ispartofNeuroscience
dc.relation.ispartofsjr1,602
dc.rights.accessRightsAcesso aberto
dc.sourceScopus
dc.subjecthindbrain
dc.subjectHSD2 neurons
dc.subjectmineralocorticoids
dc.subjectsodium appetite
dc.titleRapid stimulation of sodium intake combining aldosterone into the 4th ventricle and the blockade of the lateral parabrachial nucleusen
dc.typeArtigo
unesp.author.lattes4544450092427426[7]
unesp.author.orcid0000-0002-1395-4036[7]

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