dc.contributorUniversidade Estadual Paulista (Unesp)
dc.creatorZanella, Regis C. [UNESP]
dc.creatorMelo, Mariana Rosso [UNESP]
dc.creatorFuruya, Werner Issao [UNESP]
dc.creatorColombari, Eduardo [UNESP]
dc.creatorMenani, José V. [UNESP]
dc.creatorColombari, Débora Simões Almeida [UNESP]
dc.date2015-12-07T15:40:46Z
dc.date2015-12-07T15:40:46Z
dc.date2016
dc.date.accessioned2023-09-12T07:39:31Z
dc.date.available2023-09-12T07:39:31Z
dc.identifierhttp://dx.doi.org/10.1016/j.neulet.2015.10.067
dc.identifierNeuroscience Letters, v. 610, p. 129-134, 2016.
dc.identifier1872-7972
dc.identifierhttp://hdl.handle.net/11449/131695
dc.identifier10.1016/j.neulet.2015.10.067
dc.identifier4544450092427426
dc.identifier26528792
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8780973
dc.descriptionIntragastric 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.
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionDepartment of Physiology and Pathology, School of Dentistry, São Paulo State University, UNESP, Araraquara,SP, Brazil
dc.descriptionDepartment of Physiology and Pathology, School of Dentistry, São Paulo State University, UNESP, Araraquara,SP, Brazil.
dc.format129-134
dc.languageeng
dc.publisherElsevier B. V.
dc.relationNeuroscience Letters
dc.rightsAcesso restrito
dc.sourcePubMed
dc.subjectHypertonic saline
dc.subjectOsmoreceptors
dc.subjectReactive oxygen species
dc.subjectRenal excretion
dc.subjectWater intake
dc.titleHydrogen peroxide centrally attenuates hyperosmolarity-induced thirst and natriuresis
dc.typeArtigo


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