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Anabolic steroid associated to physical training induces deleterious cardiac effects
Everton Crivoi Do Carmo1, Tiago Fernandes, Daniel Koike
1School of Physical Education and Sport, University of São Paulo, São Paulo, SP, Brazil.
Purpose:
Cardiac aldosterone might be involved in the deleterious effects of nandrolone decanoate (ND) 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 eight groups (n = 14 per group): Control (C), nandrolone decanoate (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(-1)·wk(-1)) was administered during 10 wk of swimming training (five times per week). Losartan (20 mg·kg(-1)·d(-1)) and spironolactone (10 mg·kg(-1)·d(-1)) 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 left ventricle-angiotensin-converting enzyme I activity, AT1 receptor expression, aldosterone synthase (CYP11B2), and 11-β hydroxysteroid dehydrogenase 2 (11β-HSD2) 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 left ventricle-angiotensin-converting enzyme I activity, CYP11B2, 11β-HSD2, TGFβ, and osteopontin induced by the ND treatment.
Conclusions:
We believe this is the first study to show 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.
Insights
Nandrolone decanoate (ND) causes cardiac hypertrophy and fibrosis by increasing cardiac aldosterone. Blocking aldosterone receptors with losartan or spironolactone prevented these harmful effects, highlighting aldosterone
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Pharmacology
Background:
- Nandrolone decanoate (ND) is an anabolic steroid known to have adverse cardiovascular effects.
- Cardiac aldosterone may play a role in the detrimental impact of ND on the heart.
- Understanding the mechanisms behind ND-induced cardiac dysfunction is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the involvement of cardiac aldosterone in nandrolone decanoate-induced cardiac hypertrophy and fibrosis.
- To determine if blocking AT1 or mineralocorticoid receptors can mitigate the adverse cardiac effects of ND.
Main Methods:
- Male Wistar rats were divided into eight groups, including control, ND, trained, and trained ND groups.
- Animals received ND (10 mg·kg⁻¹·wk⁻¹) for 10 weeks, with some undergoing swimming training.
- Pharmacological blockade was achieved using losartan (AT1 receptor antagonist) or spironolactone (mineralocorticoid receptor antagonist) administered in drinking water.
Main Results:
- ND treatment significantly increased cardiac hypertrophy and collagen volumetric fraction (CVF), with a further increase observed in trained ND rats.
- ND elevated left ventricle angiotensin-converting enzyme I activity, AT1 receptor expression, aldosterone synthase (CYP11B2), 11-β hydroxysteroid dehydrogenase 2 (11β-HSD2), TGFβ, and osteopontin.
- Both losartan and spironolactone effectively inhibited ND-induced increases in CVF, collagen type III, and the measured molecular markers.
Conclusions:
- This study provides the first evidence linking cardiac aldosterone to the adverse cardiac effects of nandrolone decanoate.
- The findings suggest that cardiac aldosterone mediates ND-induced cardiac hypertrophy and fibrosis, potentially through TGFβ and osteopontin pathways.
- Pharmacological inhibition of AT1 or mineralocorticoid receptors can prevent ND-induced cardiac damage, underscoring the role of the cardiac renin-angiotensin-aldosterone system.
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