title: The role of the reduction of spiral artery remodeling and heme oxygenase 1 in mediating AT1-AA-induced hypertension and intrauterine growth restriction in pregnant rats.
abstract: BACKGROUND
  Recently, emerging evidence has indicated that preeclamptic women who have angiotensin receptor agonistic autoantibodies (AT1-AA), these antibodies contribute to features of the disease.
  
  
  OBJECTIVE
  The purpose of this study was to determine the role of spiral artery remodeling in mediating AT1-AA-induced hypertension and intrauterine growth restriction in pregnant rats. We hypothesized that AT1-AA-mediated heme oxygenase 1 (HO-1) reduction contributes to decreased spiral artery remodeling. Rat AT1-AA and an HO-1 inducer were administered to pregnant rats.
  
  
  RESULTS
  Mean arterial pressure (MAP) increased from 98 ± 4 mm Hg in normal pregnant rats to 113 ± 6 mm Hg in AT1-AA-infused rats (p < 0.05), which was significantly attenuated by the HO-1 inducer (103 ± 2 mm Hg). Fetal weight was also attenuated by HO-1 inducer, and kidney and liver development was adversely affected. Spiral artery remodeling was significantly reduced in AT1-AA-treated pregnant rats compared with that in normal pregnant rats, and this was significantly ameliorated by an HO-1 inducer.
  
  
  CONCLUSIONS
  Our findings demonstrate that AT1-AA-mediated HO-1 reduction contributes to reduced spiral artery remodeling, and is one mechanism whereby AT1-AA mediates hypertension and intrauterine growth retardation.
authors.affiliation: Department of Obstetrics and Gynaecology, Shengjing Hospital of China Medical University, Shenyang, China.
authors.forename: Dan
authors.initials: D
authors.lastname: Zhang
authors.affiliation: Department of Obstetrics and Gynaecology, Shengjing Hospital of China Medical University, Shenyang, China.
authors.forename: Leilei
authors.initials: L
authors.lastname: Wang
authors.affiliation: Department of Obstetrics and Gynaecology, Shengjing Hospital of China Medical University, Shenyang, China.
authors.forename: Chong
authors.initials: C
authors.lastname: Qiao
authors.affiliation: Department of Obstetrics and Gynaecology, Shengjing Hospital of China Medical University, Shenyang, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Yu
authors.affiliation: Department of Obstetrics and Gynaecology, Beijing Ditan Hospital Capital Medical University, Beijing, China.
authors.forename: Lihua
authors.initials: L
authors.lastname: Fu
authors.affiliation: Department of Obstetrics and Gynaecology, Shengjing Hospital of China Medical University, Shenyang, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Shang
mesh_terms: D000818:Animals; D062186:Arterial Pressure / Q000187:drug effects*; D001158:Arteries / Q000503:physiopathology; D001323:Autoantibodies / Q000494:pharmacology*; D020536:Enzyme Activators / Q000494:pharmacology; D005260:Female; D005317:Fetal Growth Retardation / Q000139:chemically induced / Q000378:metabolism*; D051547:Heme Oxygenase-1 / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D006427:Hemin / Q000494:pharmacology; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism*; D007668:Kidney / Q000187:drug effects / Q000196:embryology; D008099:Liver / Q000187:drug effects / Q000196:embryology; D010920:Placenta / Q000737:chemistry / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D044140:Receptor, Angiotensin, Type 1 / Q000819:agonists / Q000276:immunology*; D066253:Vascular Remodeling
chemical_list: D001323:Autoantibodies; D020536:Enzyme Activators; D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D006427:Hemin; D051547:Heme Oxygenase-1