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Exercise induces renin-angiotensin system unbalance and high collagen expression in the heart of Mas-deficient mice

Item Type:Article
Title:Exercise induces renin-angiotensin system unbalance and high collagen expression in the heart of Mas-deficient mice
Creators Name:Guimaraes, G.G. and Santos, S.H.S. and Oliveira, M.L. and Pimenta-Veloso, E.P. and Motta, D.F. and Martins, A.S. and Alenina, N. and Bader, M. and Santos, R.A.S. and Campagnole-Santos, M.J.
Abstract:The renin-angiotensin system (RAS) is involved in the cardiac and vascular remodeling associated with cardiovascular diseases. Angiotensin (Ang) II/AT(1) axis is known to promote cardiac hypertrophy and collagen deposition. In contrast, Ang-(1-7)/Mas axis opposes Ang II effects in the heart producing anti-trophic and anti-fibrotic effects. Exercise training is known to induce cardiac remodeling with physiological hypertrophy without fibrosis. We hypothesize that cardiac remodeling induced by chronic exercise depends on the action of Ang-(1-7)/Mas axis. Thus, we evaluated the effect of exercise training on collagen deposition and RAS components in the heart of FVB/N mice lacking Mas receptor (Mas-KO). Male wild-type and Mas-KO mice were subjected to a moderate-intense swimming exercise training for 6 weeks. The left ventricle (LV) of the animals was sectioned and submitted to qRT-PCR and histological analysis. Circulating and tissue angiotensin peptides were measured by RIA. Sedentary Mas-KO presented a higher circulating Ang II/Ang-(1-7) ratio and an increased ACE2 expression in the LV. Physical training induced in Mas-KO and WT a similar cardiac hypertrophy accompanied by a pronounced increase in collagen I and III mRNA expression. Trained Mas-KO and trained WT presented increased Ang-(1-7) in the blood. However, only in trained-WT there was an increase in Ang-(1-7) in the LV. In summary, we showed that deletion of Mas in FVB/N mice produced an unbalance in RAS equilibrium increasing Ang II/AT(1) arm and inducing deleterious cardiac effects as deposition of extracellular matrix proteins. These data indicate that Ang-(1-7)/Mas axis is an important counter-regulatory mechanism in physical training mediate cardiac adaptations.
Keywords:Angiotensin-(1-7), Mas Receptor, Exercise Training, Extracellular Matrix Proteins, Collagen, Renin-Angiotensin System, Animals, Mice
Page Range:54-61
Date:November 2012
Official Publication:https://doi.org/10.1016/j.peptides.2012.05.024
PubMed:View item in PubMed

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