Efeitos da lesão do núcleo septal intermediário sobre a ingestão de água e parâmetros cardiovasculares em ratos induzidas por diferentes protocolos

• Ano de defesa: 2006
• Autor(a) principal: Freiria-Oliveira, André Henrique
• Orientador(a): Saad, Wilson Abrão
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de São Carlos
• Programa de Pós-Graduação: Programa Interinstitucional de Pós-Graduação em Ciências Fisiológicas - PIPGCF
• País: BR
• Palavras-chave em Português: Medicina experimental - rato; Área septal; Ingestão de água; Desidratação celular e extracelular; Equilíbrio hidro-eletrolítico (Fisiologia)
• Palavras-chave em Inglês: Lateral septal intermediate nucleus; Water intake; Cardiovascular change; Angiotensinergic and cholinergic pathways
• Área do conhecimento CNPq: CIENCIAS BIOLOGICAS::FISIOLOGIA
• Link de acesso: https://repositorio.ufscar.br/handle/20.500.14289/1280

The involvement of the septal area in important regulatory mechanisms of water intake and cardiovascular adjustments has been shown by several studies. The aim of this work is to study the involvement of a subdivision of the lateral septal area on dipsogenic and cardiovascular adjustments. The effects of lateral septal intermediate nucleus lesions (LSI) on the water intake induced by different protocols, like angiotensin II and carbachol microinjected into the lateral ventricle, water deprivation by twenty four hours, intragastric hypertonic load and subcutaneous isoproterenol were investigated. We also studied the role of the LSI in cardiovascular changes induced by angiotensin II and carbachol microinjections into the lateral ventricle. Our results showed that the LSI rats did not alter body weight and did not alter the daily water intake when compared to the sham group. The LSI lesions affected the water intake induced by angiotensin II (7.6 ± 1.15 vs Sham: 17.01 ± 1.07 ml/60 min) and that induced by carbachol (9.58 ± 1.51 vs Sham: 13.62 ± 1.96 ml/60 min), as well as affected the pressor response produced by angiotensina II (∆  21.3 ± 1.5 vs Sham: ∆ 30.1 ± 2.5 mmHg) or induced by carbachol (∆ 39.0 ± 2.6 mmHg vs Sham: ∆ 49.9 ± 3.2 mmHg) into the lateral ventricle. The LSI lesions decreased dipsogenic responses after water deprivation (18.18 ± 0.81 vs Sham: 21.78± 1.23 ml/120 min) and after subcutaneus isoproterenol (5.4 ± 0.4 vs Sham: 8.4 ± 0.6 ml/120 min), but they did not decrease the water intake after intragastric hypertonic NaCl load (10.5 ± 0.47 vs Sham: 11.56 ± 1.24 ml/120 min). Thus, our results suggest the involvement of LSI through cholinergic and angiotensinergic mechanisms, as well as the central osmoreceptors activation, which possibly act by modulating the hypothalamic nucleus activity in both water intake and cardiovascular adjustments.