Hydrogen peroxide centrally attenuates hyperosmolarity-induced thirst and natriuresis

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dc.contributor.authorZanella, Regis C. [UNESP]
dc.contributor.authorMelo, Mariana Rosso [UNESP]
dc.contributor.authorFuruya, Werner Issao [UNESP]
dc.contributor.authorColombari, Eduardo [UNESP]
dc.contributor.authorMenani, José V. [UNESP]
dc.contributor.authorColombari, Débora Simões Almeida [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2015-12-07T15:40:46Z
dc.date.available2015-12-07T15:40:46Z
dc.date.issued2016
dc.description.abstractIntragastric hypertonic NaCl that simulates the ingestion of osmotically active substances by food intake induces thirst, vasopressin and oxytocin release, diuresis and natriuresis. Reactive oxygen species (ROS) produced endogenously in central areas may act modulating autonomic and behavioral responses. In the present study, we investigated the effects of H2O2 injected centrally on water intake and renal responses induced by increasing plasma osmolality with intragastric (ig) administration of 2M NaCl (2ml/rat). Male Holtzman rats (280-320g) with stainless steel cannula implanted in the lateral ventricle (LV) were used. Injections of H2O2 (2.5μmol/1μl) into the LV reduced ig 2M NaCl-induced water intake (3.1±0.7, vs. PBS: 8.6±1.0ml/60min, p < 0.05), natriuresis (769±93, vs. PBS: 1158±168μEq/120min, p<0.05) and diuresis (4.1±0.5, vs. PBS: 5.0±0.5ml/120min, p<0.05). Injections of H2O2 into the LV also decreased meal associated water intake (4.9±1.5, vs. PBS: 11.0±1.7ml/120min). However, H2O2 into the LV did not modify 2% sucrose intake (3.3±1.5, vs. PBS: 5.4±2.3ml/120min) or 24h food deprivation-induced food intake (8.2±2.0, vs. PBS: 11.0±1.6g/120min), suggesting that this treatment does not produce nonspecific inhibition of ingestive behaviors. The data suggest an inhibitory role for H2O2 acting centrally on thirst and natriuresis induced by hyperosmolarity and on meal-associated thirst.en
dc.description.affiliationDepartment of Physiology and Pathology, School of Dentistry, São Paulo State University, UNESP, Araraquara,SP, Brazil
dc.description.affiliationUnespDepartment of Physiology and Pathology, School of Dentistry, São Paulo State University, UNESP, Araraquara,SP, Brazil.
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent129-134
dc.identifierhttp://dx.doi.org/10.1016/j.neulet.2015.10.067
dc.identifier.citationNeuroscience Letters, v. 610, p. 129-134, 2016.
dc.identifier.doi10.1016/j.neulet.2015.10.067
dc.identifier.issn1872-7972
dc.identifier.lattes4544450092427426
dc.identifier.pubmed26528792
dc.identifier.urihttp://hdl.handle.net/11449/131695
dc.language.isoeng
dc.publisherElsevier B. V.
dc.relation.ispartofNeuroscience Letters
dc.rights.accessRightsAcesso restrito
dc.sourcePubMed
dc.subjectHypertonic salineen
dc.subjectOsmoreceptorsen
dc.subjectReactive oxygen speciesen
dc.subjectRenal excretionen
dc.subjectWater intakeen
dc.titleHydrogen peroxide centrally attenuates hyperosmolarity-induced thirst and natriuresisen
dc.typeArtigo
dcterms.rightsHolderElsevier B. V.
unesp.author.lattes4544450092427426[4]
unesp.author.orcid0000-0002-1395-4036[4]
unesp.author.orcid0000-0003-1167-4441[5]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araraquarapt

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