Anabolic Steroid Associated to Physical Training Induces Deleterious Cardiac Effects

Male 0301 basic medicine Heart Ventricles Cardiomegaly Stroke Volume Peptidyl-Dipeptidase A Spironolactone Losartan Receptor, Angiotensin, Type 1 Rats 3. Good health 03 medical and health sciences Anabolic Agents Collagen Type III 0302 clinical medicine 11-beta-Hydroxysteroid Dehydrogenase Type 2 Animals Cytochrome P-450 CYP11B2 Nandrolone Rats, Wistar Angiotensin II Type 1 Receptor Blockers Swimming Mineralocorticoid Receptor Antagonists
DOI: 10.1249/mss.0b013e318217e8b6 Publication Date: 2011-03-29T05:57:02Z
ABSTRACT
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.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.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.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.
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