Cardiac AT1 receptor-dependent and IGF1 receptor-independent signaling is activated by a single bout of resistance exercise

Title:

Cardiac AT1 receptor-dependent and IGF1 receptor-independent signaling is activated by a single bout of resistance exercise

Creator:

Melo, S. F. S., Barauna, V. G., Fernandes, T., Carmo, E. C., Carvalho, C. R. O., and Oliveira, E. M.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:b3d33904-c631-422b-9517-5aef9b38add2
uuid:b3d33904-c631-422b-9517-5aef9b38add2

Subject:

AT1 receptor, cardiac hypertrophy, β-arrestin, and resistance exercise

Type:

article, model:article, and TEXT

Description:

AT1 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 β-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 β-arrestin-dependent pathway.

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2017 Volume:66 | Number:6

Harvested from:

CDK

Metadata only:

false