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dc.contributor.authorPedrino, Gustavo Rodrigues
dc.contributor.authorFreiria-Oliveira, Andre Henrique
dc.contributor.authorAlmeida Colombari, Debora Simoes
dc.contributor.authorRosa, Daniel Alves
dc.contributor.authorCravo, Sergio Luiz [UNIFESP]
dc.date.accessioned2016-01-24T14:27:15Z
dc.date.available2016-01-24T14:27:15Z
dc.date.issued2012-05-21
dc.identifierhttp://dx.doi.org/10.1371/journal.pone.0037587
dc.identifier.citationPlos One. San Francisco: Public Library Science, v. 7, n. 5, 9 p., 2012.
dc.identifier.issn1932-6203
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/34899
dc.description.abstractRenal vasodilation and sympathoinhibition are recognized responses induced by hypernatremia, but the central neural pathways underlying such responses are not yet entirely understood. Several findings suggest that A2 noradrenergic neurons, which are found in the nucleus of the solitary tract (NTS), play a role in the pathways that contribute to body fluid homeostasis and cardiovascular regulation. the purpose of this study was to determine the effects of selective lesions of A2 neurons on the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Male Wistar rats (280-350 g) received an injection into the NTS of anti-dopamine-beta-hydroxylase-saporin (A2 lesion; 6.3 ng in 60 nl; n = 6) or free saporin (sham; 1.3 ng in 60 nl; n = 7). Two weeks later, the rats were anesthetized (urethane 1.2 g.kg(-1) b.wt., i.v.) and the blood pressure, renal blood flow (RBF), renal vascular conductance (RVC) and renal sympathetic nerve activity (RSNA) were recorded. in sham rats, the HS infusion (3 M NaCl, 1.8 ml.kg(-1) b.wt., i.v.) induced transient hypertension (peak at 10 min after HS; 9 +/- 2.7 mmHg) and increases in the RBF and RVC (141 +/- 7.9% and 140 +/- 7.9% of baseline at 60 min after HS, respectively). HS infusion also decreased the RSNA (-45 +/- 5.0% at 10 min after HS) throughout the experimental period. in the A2-lesioned rats, the HS infusion induced transient hypertension (6 +/- 1.4 mmHg at 10 min after HS), as well as increased RBF and RVC (133 +/- 5.2% and 134 +/- 6.9% of baseline at 60 min after HS, respectively). However, in these rats, the HS failed to reduce the RSNA (115 +/- 3.1% at 10 min after HS). the extent of the catecholaminergic lesions was confirmed by immunocytochemistry. These results suggest that A2 noradrenergic neurons are components of the neural pathways regulating the composition of the extracellular fluid compartment and are selectively involved in hypernatremia-induced sympathoinhibition.en
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFundacao de Amparo a Pesquisa do Estado de Goias (FAPEG)
dc.format.extent9
dc.language.isoeng
dc.publisherPublic Library Science
dc.relation.ispartofPlos One
dc.rightsAcesso aberto
dc.titleA2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Ratsen
dc.typeArtigo
dc.contributor.institutionUniversidade Federal de Goiás (UFG)
dc.contributor.institutionSão Paulo State Univ
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.description.affiliationUniv Fed Goias, Dept Physiol Sci, Goiania, Go, Brazil
dc.description.affiliationSão Paulo State Univ, Sch Dent, Dept Physiol & Pathol, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Dept Physiol, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Dept Physiol, São Paulo, Brazil
dc.description.sponsorshipIDCAPES: BEX1380/07-9
dc.description.sponsorshipIDCNPq: 477832/2010-5
dc.description.sponsorshipIDFundacao de Amparo a Pesquisa do Estado de Goias (FAPEG): 200910267000352
dc.identifier.fileWOS000305343100039.pdf
dc.identifier.doi10.1371/journal.pone.0037587
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000305343100039


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