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A session of strength exercise induced cardiac hypertrophy by AT1 receptor‐AKT‐mTOR signaling pathway
Author(s) -
Soares Melo Stéphano Freitas,
Amadeu Marco Aurélio,
Fernandes Tiago,
Carmo Everton Crivoi,
Magalhães Flávio Castro,
Mendes Barreti Diego Lopes,
Reno Socci Ursula Paula,
Alves Cleber Rener,
Roque Redondo Fernanda Roberta,
Brum Patrícia Chakur,
Oliveira Edilamar Menezes
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.622.1
Subject(s) - losartan , angiotensin ii receptor type 1 , protein kinase b , pi3k/akt/mtor pathway , angiotensin ii , muscle hypertrophy , phosphorylation , medicine , endocrinology , mapk/erk pathway , p70 s6 kinase 1 , receptor , signal transduction , chemistry , biochemistry
The angiotensin II type I (AT1) receptor has an important participation in the development of cardiac hypertrophy (CH). Previously, we showed that AT1 receptor participates in the cardiac hypertrophy induced by resistance training in rats (Barauna, et. al., 2008). We studied AT1 receptor signaling pathways related to the CH in rats submitted to a session of resistance exercise (SRE). Male Wistar rats were divided into six groups: control (CO); exercised and killed 5 minutes after exercise (Ex 5); exercised and killed 30 minutes after exercise (Ex 30); control treated with Losartan (CO Los); treated with Losartan, exercised and killed 5 minutes after the exercise (Ex Los 5); treated with Losartan, exercised and killed 30 minutes after training (Ex Los 30). The exercise consisted of 4 sets of 12 repetitions with 80% overload of work. The results show that phosphorylation activity of AKT in group Ex 5 and Ex 30 increased 63% and 62%, respectively, compared to CO, whereas the phosphorylation of mTOR and ERK 1/2 was increased 65% and 59%, respectively, compared to CO, only in the group Ex 30. Furthermore, these effects were blocked by losartan treatment in groups Ex Los 5 and Ex Los 30. However, to JNK1/2, p38 and p70 S6K proteins it were not observe any difference between the groups. These results, together with ours previous data shows that the AT1 receptor has an role in the activation of AKT pathway/mTOR and ERK 1/2 after a SRE.