Maternal hyperthyroidism increases the susceptibility of rat adult offspring to cardiovascular disorders

Mol Cell Endocrinol. 2015 Nov 15:416:1-8. doi: 10.1016/j.mce.2015.08.015. Epub 2015 Aug 13.

Abstract

Suboptimal intrauterine conditions as changed hormone levels during critical periods of the development are considered an insult and implicate in physiological adaptations which may result in pathological outcomes in later life. This study evaluated the effect of maternal hyperthyroidism (hyper) on cardiac function in adult offspring and the possible involvement of cardiac Renin-Angiotensin System (RAS) in this process. Wistar dams received orally thyroxin (12 mg/L) from gestational day 9 (GD9) until GD18. Adult offspring at postnatal day 90 (PND90) from hyper dams presented increased SBP evaluated by plethysmography and worse recovery after ischemia-reperfusion (I/R), as evidenced by decreased LVDP, +dP/dT and -dP/dT at 25 min of reperfusion and by increased infarct size. Increased cardiac Angiotensin I/II levels and AT1R in hyper offspring were verified. Herein, we provide evidences that maternal hyperthyroidism leads to altered expression of RAS components in adult offspring, which may be correlated with worse recovery of the cardiac performance after ischemic insults and hypertension.

Keywords: Cardiac renin-angiotensin system; Fetal programming; Gestational hyperthyroidism.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angiotensin I / metabolism
  • Angiotensin II / metabolism
  • Animals
  • Animals, Newborn
  • Disease Models, Animal
  • Disease Susceptibility
  • Female
  • Hypertension / etiology*
  • Hyperthyroidism / metabolism*
  • Male
  • Myocardial Reperfusion Injury / etiology*
  • Plethysmography
  • Pregnancy
  • Pregnancy Complications / metabolism*
  • Rats
  • Rats, Wistar
  • Receptor, Angiotensin, Type 1 / metabolism
  • Renin-Angiotensin System*
  • Thyroxine / adverse effects
  • Thyroxine / metabolism*

Substances

  • Receptor, Angiotensin, Type 1
  • Angiotensin II
  • Angiotensin I
  • Thyroxine