title: Role of reactive oxygen species in hypertension produced by reduced uterine perfusion in pregnant rats.
abstract: BACKGROUND
  Although recent studies indicate preeclampsia (PE) is associated with increased oxidative stress, the role of reactive oxygen species in the hypertension associated with PE remains unclear. We sought to test the hypothesis that placental ischemia increases oxidative stress which in turn, contributes to hypertension.
  
  
  METHODS
  Reduction in uterine perfusion pressure (RUPP) was induced by placing silver clips on the abdominal aorta and the ovarian arteries on day 14 of pregnancy. On day 20 of pregnancy, mean arterial pressure (MAP) was measured and oxidative stress was assessed in renal and placental tissues whereas systemic administration of tempol, a superoxide dismutase (SOD) mimetic, was used to evaluate the contribution of reactive oxygen species on RUPP-induced hypertension.
  
  
  RESULTS
  MAP (120 +/- 2 mm Hg vs.106 +/- 3 mm Hg), placental levels of 8-isoprostane (1.9 +/- 0.4 ng/g tissue vs. 0.8 +/- 0.1 ng/g tissue), and malondialdehyde (MDA) (6.9 +/- 0.6 micromol/g tissue vs. 3.9 +/- 0.4 micromol/g tissue) were increased, whereas renal cortical SOD activity was decreased in RUPP rats (1.2 +/- 0.1 units/mg protein vs. 1.6 +/- 0.1 units/mg protein) at day 20 of gestation (20 dG) compared to controls. Chronic treatment with tempol attenuated the hypertension (RUPP + tempol 112 +/- 2 mm Hg vs. RUPP, 120 +/- 2 mm Hg) associated with RUPP, whereas tempol had no effect on MAP (NP, 106 +/- 3 vs. NP + tempol, 108 +/- 2) in control rats.
  
  
  CONCLUSIONS
  The results of this study indicate that placental ischemia decreases innate antioxidant activity resulting in elevated oxidative stress which appears to play a role in mediating hypertension associated with chronic RUPP in pregnant rats.
authors.affiliation: Department of Physiology and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi, USA.
authors.forename: Mona
authors.initials: M
authors.lastname: Sedeek
authors.forename: Jeffrey S
authors.initials: JS
authors.lastname: Gilbert
authors.forename: Babbette B
authors.initials: BB
authors.lastname: LaMarca
authors.forename: Myssara
authors.initials: M
authors.lastname: Sholook
authors.forename: Derrick L
authors.initials: DL
authors.lastname: Chandler
authors.forename: Yuping
authors.initials: Y
authors.lastname: Wang
authors.forename: Joey P
authors.initials: JP
authors.lastname: Granger
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D004195:Disease Models, Animal; D005260:Female; D006973:Hypertension / Q000378:metabolism* / Q000503:physiopathology; D007511:Ischemia / Q000378:metabolism / Q000503:physiopathology; D018384:Oxidative Stress / Q000502:physiology*; D010920:Placenta / Q000098:blood supply* / Q000378:metabolism; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000378:metabolism* / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism*; D014599:Uterus / Q000098:blood supply*
chemical_list: D017382:Reactive Oxygen Species