Maternal hypertensive condition alters adipose tissue function and blood pressure sensitivity in offspring

Ren Ozawa1, Hisataka Iwata1, Takehito Kuwayama1

  • 1Laboratory of Animal Reproduction, Department of Animal Science, Tokyo University of Agriculture, 1737 Funako, Atsugi, Kanagawa, 234-0034, Japan.

Insights

Maternal hypertension during pregnancy, induced by angiotensin II (Ang II), leads to placental dysfunction and fetal growth restriction. Offspring exhibit altered lipid metabolism and elevated blood pressure, indicating long-term health impacts.

Area of Science:

  • Reproductive biology
  • Developmental biology
  • Cardiovascular physiology

Background:

  • Preeclampsia (PE) involves maternal hypertension and can impact fetal development.
  • The intrauterine environment under hypertensive conditions may influence offspring health.
  • Lipid metabolism and blood pressure regulation are critical for long-term health.

Purpose of the Study:

  • To investigate the effects of maternal hypertension on male offspring growth, focusing on lipid metabolism and blood pressure.
  • To determine how angiotensin II (Ang II)-induced maternal hypertension in mice impacts placental function and fetal development.
  • To assess the long-term consequences of this intrauterine environment on offspring adipocyte function and cardiovascular health.

Main Methods:

  • Induction of maternal hypertension in female mice using angiotensin II (Ang II) infusion from gestational day 12.
  • Analysis of placental lipid dysregulation and fetal growth restriction.
  • Assessment of birth weight and body weight changes in offspring.
  • Evaluation of Pparγ mRNA expression in adipocytes from neonatal and adult offspring.
  • Measurement of basal blood pressure and sensitivity to hypertensive stimuli in adult offspring.

Main Results:

  • Ang II-induced maternal hypertension caused placental lipid dysregulation and fetal growth restriction, resulting in lower birth weight in offspring.
  • Neonatal and adult offspring from hypertensive dams exhibited higher Pparγ mRNA expression in adipose tissue.
  • Adult offspring showed increased neutrophils and inflammatory monocytes in adipose tissue.
  • Ang II-offspring displayed higher basal blood pressure and increased sensitivity to hypertensive stimuli compared to controls.
  • While initially lighter, Ang II-offspring body weight caught up to controls by 16 weeks.

Conclusions:

  • Maternal hypertension induced by Ang II disrupts placental function, leading to fetal growth restriction and lower birth weight.
  • The altered intrauterine environment impacts offspring adipocyte function, characterized by increased Pparγ expression and inflammation.
  • Offspring exposed to maternal hypertension exhibit long-term cardiovascular effects, including elevated blood pressure and heightened sensitivity to hypertensive challenges.

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