title: Fetal hypoxia results in programming of aberrant angiotensin ii receptor expression patterns and kidney development.
abstract: OBJECTIVE
  The present study tested the hypothesis that fetal hypoxia adversely affects kidney development in fetal and offspring rats and alter the expression patterns of angiotensin II type 1 (AT1R) and type 2 (AT2R) receptors.
  
  
  METHODS
  Time-dated pregnant rats were divided between normoxic and hypoxic (10.5% O2 last period of gestation) groups. Protein expression, in the offspring, was determined using western blot.
  
  
  RESULTS
  Hypoxic treatment significantly decreased body and kidney weight in 21-day fetuses (E21) and 7-day neonates (P7). In 3-month-old offspring there were no significant differences in body and kidney weight between hypoxic and control animals. Fetal hypoxia had no effect on kidney AT1R density in E21 or P7, but significantly decreased kidney AT1R protein and mRNA abundance in both male and female adults. In contrast, kidney AT2R density was not affected by fetal hypoxia throughout the developmental stages studied. The hypoxia-mediated reduction of nephron numbers was progressively from P7 worsened into the adulthood with females affected more than males.
  
  
  CONCLUSIONS
  The results suggest that fetal hypoxia causes programming of aberrant kidney development and accelerates the aging process of the kidney during the postnatal development, which may contribute to an increased risk of cardiovascular disease.
authors.affiliation: Center for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, CA, 92350, USA.
authors.forename: Pablo
authors.initials: P
authors.lastname: Gonzalez-Rodriguez
authors.forename: Wenni
authors.initials: W
authors.lastname: Tong
authors.forename: Qin
authors.initials: Q
authors.lastname: Xue
authors.forename: Yong
authors.initials: Y
authors.lastname: Li
authors.forename: Shirley
authors.initials: S
authors.lastname: Hu
authors.forename: Lubo
authors.initials: L
authors.lastname: Zhang
mesh_terms: D000818:Animals; D002318:Cardiovascular Diseases / Q000209:etiology / Q000473:pathology; D047108:Embryonic Development / Q000235:genetics; D005260:Female; D005311:Fetal Hypoxia; D018507:Gene Expression Regulation, Developmental; D007668:Kidney / Q000254:growth & development / Q000378:metabolism / Q000473:pathology*; D008297:Male; D009399:Nephrons / Q000254:growth & development / Q000473:pathology; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics* / Q000378:metabolism; D044139:Receptor, Angiotensin, Type 2 / Q000235:genetics* / Q000378:metabolism; D012307:Risk Factors
chemical_list: D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2
keywords: AT1R; AT2R; Rats; nephron number; sex.