Mediação neural na hipotensão pós-exercício em ratos hipertensos

Detalhes bibliográficos
Ano de defesa: 2014
Autor(a) principal: Barreto, André Sales lattes
Orientador(a): Santos, Márcio Roberto Viana dos lattes
Banca de defesa: Não Informado pela instituição
Tipo de documento: Tese
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de Sergipe
Programa de Pós-Graduação: Pós-Graduação em Ciências da Saúde
Departamento: Não Informado pela instituição
País: BR
Palavras-chave em Português:
Palavras-chave em Inglês:
Área do conhecimento CNPq:
Link de acesso: https://ri.ufs.br/handle/riufs/3565
Resumo: The sustained reduction in blood pressure after a single bout of aerobic or resistance exercise (RE) has gained significant clinical relevance in hypertensive individuals. This phenomenon is known as post-exercise hypotension (PEH). However, the neural mechanisms that lead to HPE still need to be better understood, particularly arising from the ER. In this sense, the present study sought to review the neural mechanisms involved in HPE and evaluate the hemodynamic and autonomic control changes induced by ER in hypertensive rats induced by Nω-nitro-Larginine methyl ester (L-NAME). The thesis consists of two chapters, which are systematic review and an original article. Initially was elaborated a systematic review "A systematic review of neural mechanisms involved on post-exercise hypotension in hypertensive animals", with search for articles in LILACS, EMBASE and PUBMED database, which describes an overview of the neural mechanisms involved in HPE in studies of hypertensive animals. These studies demonstrated the presence of cardiovascular afferents, afferent skeletal muscle stimulation during exercise and bulbar or suprabulbar modulations are fundamental to the expression of HPE. After completion of the experimental protocols the article: "Arterial Baroreflex participates in the post-resistance exercise hypotension in L-NAME-induced hypertensive rats", was presented. This paper demonstrated that the increased baroreflex arterial sensitibity REinduced plays a crucial role in PEH followed by bradycardia, probably through cardiac and vascular sympathetic inhibition. Together, these findings show that the involvement of neural mechanisms are important for the manifestation of PEH induced by both aerobic and resistance exercise in hypertensive rats.