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Voluntary exercise during 6 weeks induces pathological cardiovascular responses in MAS‐deficient mice (881.4)
Author(s) -
Santos Daisy,
Santos Robson,
Oliveira Marilene,
Mosienko Valentina,
Plehm Ralph,
Todiras Mihail,
Qadri Fatimunnisa,
Poglitsch Marko,
Alenitasha,
Bader Michael
Publication year - 2014
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.28.1_supplement.881.4
Subject(s) - endocrinology , medicine , skeletal muscle , aerobic exercise , muscle hypertrophy , angiotensin ii , ventricle , adipose tissue , apelin , gene expression , renin–angiotensin system , fndc5 , receptor , chemistry , blood pressure , gene , extracellular matrix , biochemistry , fibronectin
Physical training induces numerous physiological adaptations in the cardiovascular and skeletal muscle system related to changes in gene expression including modulation of the renin angiotensin system (RAS) components. Thus, the aim of this study was to evaluate the effect of running wheel training in knockout mice for the angiotensin‐(1‐7) receptor (MAS‐KO). For this we used C57Bl6 male mice (8‐12 weeks old) WT and MAS‐ KO divided into voluntary exercise group or sedentary control (N = 4‐8 per group). The aerobic training lasted 6 weeks and the amount of exercise was measured by the number of rotations per day. The gene expression responses of factors related to physiological and pathological adaptations and RAS components in the left ventricle, skeletal muscle and adipose tissue were evaluated by real‐time PCR (qPCR). Blood pressure (BP) was measured before and during the period of physical training using radio‐telemetry. The plasma levels of angiotensin peptides were determined by mass spectrometry. The results showed that in WT and MAS‐KO mice aerobic training promotes cardiac hypertrophy but in MAS‐KO it induced the expression of genes related to pathological conditions (ANP and BNP) and high plasmatic AngII / AngI ratio (0.204 vs. 0,126 pg/ml). The chronic aerobic exercise promoted an increase in skeletal muscle expression of FNDC5, irisin precursor, only in WT. In contrast, angiotensin‐(1‐7) receptor deficiency mice showed reduced FNDC5 expression in skeletal muscle (gastrocnemius and soleus) and no differences in inguinal adipose tissue UCP1 expression, opposite responses to that observed in WT mice. The MAS‐KO group presented slightly elevated baseline mean BP (105.5 ± 6.55 vs. 98.48 ± 7.65 mmHg for MAS‐KO and WT). A paradoxal increase in BP after 4 weeks of voluntary running was observed im Mas‐deficient group. It was concluded that voluntary exercise during 6 weeks induces pathological cardiovascular responses in MAS‐KO mice. Grant Funding Source : CAPES/PROBRAL