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Med Sci Sports Exerc. 2011 Mar 10. [Epub ahead of print]
do Carmo EC, Fernandes T, Koike D, da Silva ND Junior, Mattos KC, Rosa KT, Barretti D, Soares Melo SF, Wichi RB, Irigoyen MC, de Oliveira EM.
Source
1School of Physical Education and Sport, University of São Paulo, São Paulo, SP, Brazil; 2Human Movement Laboratory, Sao Judas Tadeu University - São Paulo, SP, Brazil 3Hypertension Unit, Heart Institute, Medical School, University of São Paulo, São Paulo, SP, Brazil.
Abstract
PURPOSE:
Cardiac aldosterone might be involved in Nandrolone Decanoate (ND) deleterious effects on the heart. Therefore, we investigated the involvement of cardiac aldosterone, by the pharmacological block of AT1 or mineralocorticoid receptors, on cardiac hypertrophy and fibrosis.
METHODS:
Male Wistar rats were randomized into 8 groups (n=14/group): Control (C), Nandrolone Deconoate (ND), Trained (T), Trained ND (TND), ND+Losartan (ND +L), Trained ND +Losartan (TND +L), ND+Spironolactone (ND+S) and Trained ND+Spironolactone (TND+S). ND (10 mg/kg/week), was administered during 10 weeks of swimming training (5 times/wk). Losartan (20mg/kg/day) and Spironolactone (10mg/kg/day) were administered in drinking water.
RESULTS:
Cardiac hypertrophy was increased 10% by using ND and 17% by ND plus training (p<0.05). In both groups, there was an increase in the collagen volumetric fraction (CVF) and cardiac collagen type III expression (p<0.05). The ND treatment increased: LV-ACE activity, AT1 receptor expression, aldosterone synthase (CYP11B2) and 11-β hydroxysteroid dehydrogenase 2 (11βHSD2) gene expression and inflammatory markers, TGFβ and osteopontin. Both Losartan and Spironolactone inhibited the increase of CVF and collagen type III. In addition, both treatments inhibited the increase in LV-ACE activity, CYP11B2, 11βHSD2, TGFβ and osteopontin induce by the ND treatment.
CONCLUSION:
We believe this is the first study showing the effects of ND on cardiac aldosterone. Our results suggest that these effects may be associated to TGFβ and osteopontin. Thus, we conclude that the cardiac aldosterone has an important role on the deleterious effects on the heart induced by ND.
Med Sci Sports Exerc. 2011 Mar 10. [Epub ahead of print]
do Carmo EC, Fernandes T, Koike D, da Silva ND Junior, Mattos KC, Rosa KT, Barretti D, Soares Melo SF, Wichi RB, Irigoyen MC, de Oliveira EM.
Source
1School of Physical Education and Sport, University of São Paulo, São Paulo, SP, Brazil; 2Human Movement Laboratory, Sao Judas Tadeu University - São Paulo, SP, Brazil 3Hypertension Unit, Heart Institute, Medical School, University of São Paulo, São Paulo, SP, Brazil.
Abstract
PURPOSE:
Cardiac aldosterone might be involved in Nandrolone Decanoate (ND) deleterious effects on the heart. Therefore, we investigated the involvement of cardiac aldosterone, by the pharmacological block of AT1 or mineralocorticoid receptors, on cardiac hypertrophy and fibrosis.
METHODS:
Male Wistar rats were randomized into 8 groups (n=14/group): Control (C), Nandrolone Deconoate (ND), Trained (T), Trained ND (TND), ND+Losartan (ND +L), Trained ND +Losartan (TND +L), ND+Spironolactone (ND+S) and Trained ND+Spironolactone (TND+S). ND (10 mg/kg/week), was administered during 10 weeks of swimming training (5 times/wk). Losartan (20mg/kg/day) and Spironolactone (10mg/kg/day) were administered in drinking water.
RESULTS:
Cardiac hypertrophy was increased 10% by using ND and 17% by ND plus training (p<0.05). In both groups, there was an increase in the collagen volumetric fraction (CVF) and cardiac collagen type III expression (p<0.05). The ND treatment increased: LV-ACE activity, AT1 receptor expression, aldosterone synthase (CYP11B2) and 11-β hydroxysteroid dehydrogenase 2 (11βHSD2) gene expression and inflammatory markers, TGFβ and osteopontin. Both Losartan and Spironolactone inhibited the increase of CVF and collagen type III. In addition, both treatments inhibited the increase in LV-ACE activity, CYP11B2, 11βHSD2, TGFβ and osteopontin induce by the ND treatment.
CONCLUSION:
We believe this is the first study showing the effects of ND on cardiac aldosterone. Our results suggest that these effects may be associated to TGFβ and osteopontin. Thus, we conclude that the cardiac aldosterone has an important role on the deleterious effects on the heart induced by ND.
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