Cardiac AT(1) Receptor-Dependent and IGF1 Receptor-Independent Signaling Is Activated by a Single Bout of Resistance Exercise

Autor(es)

Melo, S. F. S. ^{[1, 2]} ; Barauna, V. G. ^[1] ; Fernandes, T. ^[2] ; Carmo, E. C. ^[2] ; Carvalho, C. R. O. ^[3] ; Oliveira, E. M. ^[2]

Afiliação do(s) autor(es)

^[1] Univ Fed Espirito Santo, Hlth Sci Ctr, Lab Mol Physiol, Vitoria - Brazil

^[2] Univ Sao Paulo, Lab Biochem & Mol Biol Exercise, Dept Human Movement Biodynam, Sch Phys Educ & Sport, Sao Paulo - Brazil

^[3] Univ Sao Paulo, Dept Physiol & Biophys, Lab Cellular Signaling, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Physiological Research; v. 66, n. 6, p. 1061-1065, 2017.
• Citações Web of Science: 1

Resumo

AT(1) receptor (AT1R) blockade prevents physiological cardiac hypertrophy induced by resistance training. Also, our group showed that a single bout of resistance exercise (RE) activates the AKT/mTOR which was also inhibited by AT1R blocker. Here, we investigated whether IGF1-receptor (IGF1-R) and MAPKs were also activated after a single bout of RE. Wistar rats were divided into Sedentary (Sed), Sedentary treated with losartan (Sed+LOS), Exercise (EX), and Exercise treated with losartan (EX+LOS). Cardiac tissue was obtained 5 and 30 min after 4 sets of 12 repetitions of squat exercise (80 % 1RM). We demonstrated that a single bout of RE did not induce IGF1-R tyrosine phosphorylation. ERK1/2 and P38 phosphorylation levels were elevated in the EX 5min and EX 30min groups however, only ERK1/2 was inhibited by losartan treatment (AT1R blocker). Next, we showed that beta-arrestin-2 expression increased 28 % in trained animals compared to sedentary group. Altogether, our results demonstrate that AT1R, but not IGF1-R, may exert the hypertrophic cardiac stimulus RE-induced. Also, activation of AKT/mTOR and ERK1/2 pathways may occur through the beta-arrestin-dependent pathway. (AU)

• Processo FAPESP: 07/52457-3 - Estudo da participacao do receptor de angiotensina ii na jipertrofia cardiaca induzida pelo treinamento resistido com o uso de um antisense para o receptor at1.
• Beneficiário: Stéphano Freitas Soares Melo
• Linha de fomento: Bolsas no Brasil - Mestrado
• Processo FAPESP: 10/09438-0 - UTILIZAÇÃO TERAPÊUTICA DE microRNAS RESPONSÁVEIS PELA REGULAÇÃO DA CONTRATILIDADE CARDÍACA ASSOCIADO AO TREINAMENTO FÍSICO AERÓBICO EM RATOS COM INSUFICIÊNCIA CARDÍACA
• Beneficiário: Stéphano Freitas Soares Melo
• Linha de fomento: Bolsas no Brasil - Doutorado