Ingestão e palatabilidade ao sódio relacionados aos mecanismos inibitórios do núcleo parabraquial lateral em modelos de desidratação intracelular e extracelular

• Ano de defesa: 2019
• Autor(a) principal: Cavassim, Diulie Graziela Felipe
• Orientador(a): Andrade, Carina Aparecida Fabrício de
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de São Carlos; Câmpus São Carlos
• Programa de Pós-Graduação: Programa Interinstitucional de Pós-Graduação em Ciências Fisiológicas - PIPGCF
• Palavras-chave em Português: Desidratação; Apetite ao sódio; Palatabilidade; Comportamento ingestivo; Tronco encefálico
• Palavras-chave em Inglês: Dehydration; Sodium appetite; Palatability; Ingestive behavior; Brainstem
• Área do conhecimento CNPq: CIENCIAS BIOLOGICAS::FISIOLOGIA::FISIOLOGIA DE ORGAOS E SISTEMAS::NEUROFISIOLOGIA
• Link de acesso: https://repositorio.ufscar.br/handle/20.500.14289/16472

Several evidences correlate excessive salt intake with the development or aggravation of chronic diseases, including hypertension and cerebrovascular diseases. One factor that could contribute to excessive salt intake is its ability to improve the palatability of foods. An important inhibitory mechanism for the control of sodium intake has been described for the lateral parabrachial nucleus (LPBN), structure bilaterally located in the pons. Previous studies have shown that LPBN α2-adrenergic receptors activation with bilateral injections of moxonidine produces a potent increase in extracellular dehydration-induced 0.3 M NaCl intake, prolonging the increase in sodium palatability induced by sodium depletion. Although blocking LPBN inhibitory mechanisms produces a paradoxical intake of 0.3 M NaCl in rats with intracellular dehydration, it is still unknown whether activation of α2-adrenergic receptors in LPBN could alter sodium palatability under these conditions. Here we investigated: 1) sodium palatability and appetite induced by 24 hours of water deprivation (intracellular and extracellular dehydration model), and 2) sodium palatability in rats submitted to intragastric overload (intracellular dehydration) after administration of moxonidine or vehicle in LPPN. Present results showed that in rats submitted to 2 M NaCl (2 ml/rat) intragastric overload (intracellular dehydration) unilateral administration of moxonidine (α2-adrenergic/I1 imidazoline receptors agonist) into the LPBN did not change palatability to NaCl compared to vehicle treatment, although the moxonidine-treated group showed increased 0.3 M NaCl intake. When bilaterally injected into the LPBN, moxonidine did not change 24 h water deprivation-induced sodium appetite followed by partial rehydration period when compared to vehicle treatment. However, when animals were not allowed to be partially rehydrated, i.e., they had immediate and simultaneous access to water and 0.3 M NaCl during two hours, there was a potent increase in hypertonic sodium intake after bilateral moxonidine injections into the NPBL. In another group of animals without LPBN cannulas, there was an increase in hedonic responses frequency to intra-oral infusion of 0.3 M NaCl after 24 h water deprivation in relation to basal condition (normohydration), recovering to basal values after the partial rehydration period. The present results suggest that the increase in NaCl intake, evidenced only after water deprivation period, without previous partial rehydration, could be associated with the increase of hedonic responses frequency to intraoral infusion. However, with regard to intracellular dehydration exclusively, moxonidine unilateral LPBN injections promoted an increase in 0.3 M NaCl intake without changes in palatability for this solution.