title: Testosterone improves cardiac function and alters angiotensin II receptors in isoproterenol-induced heart failure.
abstract: BACKGROUND
  The renin-angiotensin-aldosterone system is known to play an important role in the pathophysiology and development of heart failure. Several studies have reported the benefits of testosterone in heart failure. However, the mechanisms of testosterone-induced effects on heart failure require further study.
  
  
  OBJECTIVE
  To determine the effects of castration and testosterone administration on cardiac function and angiotensin II receptor function in rats with isoproterenol-induced heart failure.
  
  
  METHODS
  Wistar rats were divided randomly into control and heart failure groups. The heart failure groups were further divided into the following groups: castration; castration+testosterone replacement; and sham castration. Echocardiography and haemodynamic measurements were used to evaluate cardiac function. Cardiocyte apoptosis and fibrosis were determined using terminal deoxyribonucleotide transferase-mediated dUTP nick-end labelling (TUNEL) staining and Masson's Trichrome staining, respectively. Angiotensin II receptor (AT1 and AT2) messenger ribonucleic acid (mRNA) expression levels were assayed using real-time reverse transcriptase-polymerase chain reactions, while Western immunoblotting was used to estimate Bcl-2 protein expression levels.
  
  
  RESULTS
  Castration significantly increased cardiomyocyte apoptosis and fibrosis that was normally induced by isoproterenol (P<0.05). AT2 receptor mRNA expression in the castration group was increased and Bcl-2 protein expression was decreased compared with the castration+testosterone replacement group (P<0.05).
  
  
  CONCLUSIONS
  These data suggest that androgen therapy could play an important role in pathophysiological changes in heart failure and have beneficial effects for its treatment.
authors.affiliation: Department of Cardiovascular Medicine, First Affiliated Hospital, Harbin Medical University, China.
authors.forename: Ning-Ning
authors.initials: NN
authors.lastname: Kang
authors.forename: Lu
authors.initials: L
authors.lastname: Fu
authors.forename: Jin
authors.initials: J
authors.lastname: Xu
authors.forename: Ying
authors.initials: Y
authors.lastname: Han
authors.forename: Jun-Xian
authors.initials: JX
authors.lastname: Cao
authors.forename: Jun-Feng
authors.initials: JF
authors.lastname: Sun
authors.forename: Min
authors.initials: M
authors.lastname: Zheng
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D004195:Disease Models, Animal; D005355:Fibrosis; D006333:Heart Failure / Q000139:chemically induced / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D020249:Hormone Replacement Therapy; D020287:In Situ Nick-End Labeling; D007545:Isoproterenol; D008297:Male; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D009919:Orchiectomy; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D060888:Real-Time Polymerase Chain Reaction; D044140:Receptor, Angiotensin, Type 1 / Q000187:drug effects / Q000378:metabolism; D044139:Receptor, Angiotensin, Type 2 / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism; D020127:Recovery of Function; D012084:Renin-Angiotensin System / Q000187:drug effects*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D043343:Testosterone Propionate / Q000494:pharmacology*; D014463:Ultrasonography; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D007545:Isoproterenol; D043343:Testosterone Propionate