Envolvimento do receptor de angiotensina II tipo 1 nas alterações cardiovasculares induzidas pelo estresse crônico : comparação entre estressores homotípicos e heterotípicos

Detalhes bibliográficos
Ano de defesa: 2016
Autor(a) principal: Ferreira, Willian Costa
Orientador(a): Crestani, Carlos Cesar lattes
Banca de defesa: Não Informado pela instituição
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
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Palavras-chave em Inglês:
Área do conhecimento CNPq:
Link de acesso: https://repositorio.ufscar.br/handle/20.500.14289/7978
Resumo: Emotional stress has been recognized as a risk factor for cardiovascular diseases. Nevertheless, the mechanisms involved in the etiology of cardiovascular dysfunctions evoked by stress are still poorly understood. Thus, in the present study we investigated the involvement of angiotensin II acting in the type 1 receptor (AT1) in cardiovascular dysfunctions evoked by chronic stress in rats. For this, we compared the effect of chronic treatment with the AT1 receptor antagonist losartana (30mg/kg/day, p.o.) in the cardiovascular and autonomic changes following 10 days exposure to chronic variable stress (CVS, heterotypic stressor) and repeated restraint stress (RRS, homotypic stressor). Neither RRS nor CVS affected basal values of arterial pressure and heart rate. However, RRS increased sympathetic tone to the heart and decreased cardiac parasympathetic activity, whereas CVS decreased cardiac parasympathetic activity. Both chronic stressors also impaired the baroreflex function. All alterations in autonomic activity and the baroreflex impairment were inhibited by treatment with losartan. Complementary measurements of parameters commonly analyzed in studies investigating stress effects also indicated that CVS reduced body weight gain and increased circulating corticosterone, but these effects were not affected by losartan. In fact, CVS-evoked body weight change was even higher in losartan-treated animals. In conclusion, these findings indicate an involvement of angiotensin II/AT1 receptors in autonomic changes evoked by both homotypic and heterotypic chronic stressors. Additionally, present results suggest that increased circulating corticosterone evoked by CVS is independent of AT1 receptors, while reduction in body weight gain evoked by this heterotypic stressor is facilitated by treatment with losartan.