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Master's Dissertation
DOI
10.11606/D.39.2006.tde-07072006-151726
Document
Author
Full name
Valerio Garrone Barauna
E-mail
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2006
Supervisor
Committee
Oliveira, Edilamar Menezes de (President)
Krieger, Jose Eduardo
Ramires, Paulo Rizzo
Title in Portuguese
"Participação do sistema renina angiotensina na hipertrofia cardíaca induzida pelo treinamento resistido"
Keywords in Portuguese
Hipertrofia Cardíaca
Sistema Renina-Angiotensina
Treinamento Resistido
Abstract in Portuguese
Para avaliar a participação do Sistema Renina Angiotensina (SRA) sobre a Hipertrofia Cardíaca de ratos submetidos ao treinamento resistido foram usados 64 Ratos Wistar divididos em: Controle (CO), Treinado (TR), Controle ou Treinado tratados com Losartan (LOS; 20mg/Kg/d) e Controle ou Treinado tratados com NaCl (SAL; 1% água). Os grupos treinados realizaram quatro séries de 12 repetições, 5x/sem/8sem, com 65-75% de 1 Repetição Máxima (1RM). Hipertrofia cardíaca (HC), obtida pelo peso úmido do VE corrigida pelo Peso Corporal (PC) e pelo Ecocardiograma, foi observada no grupo TR com nenhum prejuízo da função ventricular. Tanto a atividade da ECA, sistêmica e local no coração, quanto a atividade da renina não foram alteradas pelo treinamento. Pelo Western blotting, não foi observada alteração na expressão protéica do peptídeo angiotensina II e do receptor de angiotensina II AT2 com o treinamento, mas observou-se aumento de 31,4% na expressão dos receptores de angiotensina II AT1 no grupo TR. A administração do antagonista do receptor AT1 (Losartan) preveniu a HC em resposta ao treinamento. O mesmo não foi observado com a administração do NaCl para inibir a atividade da Renina. Esses resultados sugerem que o receptor AT1 participa da HC induzida pelo treinamento resistido sem a necessidade de aumento na concentração da angiotensina II cardíaca. Um possível mecanismo seria a ativação direta dos receptores AT1 pelo estiramento mecânico dos cardiomiócitos.
Title in English
ROLE OF THE RENIN-ANGIOTENSIN SYSTEM IN RESISTANCE EXERCISE-INDUCED CARDIAC HYPERTROPHY
Keywords in English
Cardiac Hypertrophy
Renin-Angiotensin System
Resistance-training
Abstract in English
Besides the well-known effects of Ang II in stimulating pathological pressure-overload cardiac hypertrophy, little information is available regarding the role of Renin-Angiotensin-System (RAS) in the exercise training-induced cardiac hypertrophy. 64 male Wistar rats were divided into 6 groups: Sedentary, Trained, Sedentary or Trained + Losartan (20mg/Kg/d, n=7) and Sedentary or Trained + Salt (NaCl 1%). The exercise protocol was: 4 x 12 bouts, 5x/week during eight weeks, with 65-75% of 1 Repetition Maximum (1RM). Using LV weight/body weight ratio and echocardiography (ECHO) we have observed cardiac hypertrophy in the Trained group without any impairment in ventricular function. Concerning RAS, neither ACE, analyzed by fluorometric assay (systemic and local in the heart), nor Renin, by RIA, activities were altered after resistance training. In addition, using Western blotting analysis, no change was observed in cardiac Ang II and AT2 receptor levels while the AT1 receptor expression was upregulated in Trained groups by 31,4%. Administration of the AT1 receptor antagonist (losartan) prevented left ventricle hypertrophy in response to the resistance training. The administration of salt, to inhibit the renin activity, did not prevent the cardiac hypertrophy. These results suggest that the AT1 receptor participates in resistance-training-induced cardiac hypertrophy without an increase in Ang II concentration in the heart. A possible mechanism is the direct activation of the AT1 receptor by mechanical stretching of cardiomyocytes.
 
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Abstract.pdf (12.26 Kbytes)
Agradecimentos.pdf (13.83 Kbytes)
Capa.pdf (3.69 Kbytes)
Dissertacao.pdf (1.10 Mbytes)
FolhadeRosto.pdf (4.33 Kbytes)
ListadeFiguras.pdf (10.14 Kbytes)
ListadeSiglas.pdf (9.35 Kbytes)
ListadeTabelas.pdf (7.16 Kbytes)
Resumo.pdf (14.28 Kbytes)
Sumario.pdf (10.17 Kbytes)
Publishing Date
2006-07-25
 
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