title: Maternal hyperthyroidism alters the pattern of expression of cardiac renin-angiotensin system components in rat offspring.
abstract: BACKGROUND
  Changes in perinatal environment can lead to physiological, morphological, or metabolic alterations in adult life. It is well known that thyroid hormones (TH) are critical for the development, growth, and maturation of organs and systems. In addition, TH interact with the renin-angiotensin system (RAS), and both play a critical role in adult cardiovascular function. The objective of this study was to evaluate the effect of maternal hyperthyroidism on cardiac RAS components in pups during development.
  
  
  METHODS
  From gestational day nine (GD9), pregnant Wistar rats received thyroxine (T4, 12 mg/l in tap water; Hyper group) or vehicle (control group). Dams and pups were killed on GD18 and GD20.
  
  
  RESULTS
  Serum concentrations of triiodothyronine (T3) and T4 were higher in the Hyper group than in the control group dams. Cardiac hypertrophy was observed in Hyper pups on GD20. Cardiac angiotensin-converting enzyme (ACE) activity was significantly lower in Hyper pups on both GD18 and GD20, but there was no difference in Ang I/Ang II levels. Ang II receptors expression was higher in the Hyper pup heart on GD18.
  
  
  CONCLUSIONS
  Maternal hyperthyroidism is associated with alterations in fetal development and altered pattern of expression in RAS components, which in addition to cardiac hypertrophy observed on GD20 may represent an important predisposing factor to cardiovascular diseases in adult life.
authors.affiliation: Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, Brazil.
authors.forename: Caroline A
authors.initials: CA
authors.lastname: Lino
authors.forename: Caroline E R
authors.initials: CE
authors.lastname: Shibata
authors.forename: Maria Luiza M
authors.initials: ML
authors.lastname: Barreto-Chaves
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D006332:Cardiomegaly / Q000139:chemically induced*; D005260:Female; D047109:Fetal Development / Q000187:drug effects; D006980:Hyperthyroidism / Q000503:physiopathology*; D009035:Mothers; D009206:Myocardium / Q000378:metabolism; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar; D044140:Receptor, Angiotensin, Type 1 / Q000096:biosynthesis; D044139:Receptor, Angiotensin, Type 2 / Q000096:biosynthesis; D012084:Renin-Angiotensin System / Q000187:drug effects* / Q000502:physiology; D013974:Thyroxine / Q000097:blood / Q000494:pharmacology*; D014284:Triiodothyronine / Q000097:blood; D015854:Up-Regulation
chemical_list: D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D014284:Triiodothyronine; D007703:Peptidyl-Dipeptidase A; D013974:Thyroxine