title: Effects of reduced uterine perfusion pressure on blood pressure and metabolic factors in pregnant rats.
abstract: BACKGROUND
  Elements of metabolic syndrome (eg, dyslipidemia and impaired glucose metabolism) are often present in preeclamptic pregnancies. Currently it is unclear whether these metabolic aberrations presage preeclampsia, or if these manifestations result from placental ischemia and the ensuing proinflammatory state usually present in preeclampsia.
  
  
  METHODS
  The present study employed chronic reductions in uterine perfusion pressure (RUPP) to generate a rat model of pregnancy-induced hypertension (PIH) for the evaluation of fasting plasma concentrations of triglycerides (TGs), glucose, resistin, insulin, and glucose tolerance in late-gestation rats.
  
  
  RESULTS
  Mean arterial pressure was increased (130 +/- 2.1 mm Hg v 100 +/- 4.3 mm Hg; all values, mean +/- SEM), and fetal weight decreased (1.93 +/- 0.08 g v 2.19 +/- 0.06 g), in RUPP dams compared with normal pregnant (NP) control dams. Maternal fasting glucose (4.2 +/- 0.3 mmol L(-1) v 3.1 +/- 0.4 mmol L(-1); P < .05) was increased in RUPP compared with NP dams. Serum TGs (2.62 +/- 0.29 mmol L(-1) v 2.45 +/- 0.51 mmol L(-1)), insulin (9.9 +/- 0.7 microU mL(-1) v 8.5 +/- 0.7 microU mL(-1)), resistin (46.25 +/- 4.19 pg mL(-1) v 49.71 +/- 4.01 pg mL(-1)), and glucose area under the curve (650 +/- 35 mmol min L(-1) v 570 +/- 34 mmol min L(-1)) were not different between the RUPP and NP dams.
  
  
  CONCLUSIONS
  Although these findings do not rule out the hypothesis that preexisting symptoms of metabolic syndrome may contribute to the onset of preeclampsia, these data clearly show that pregnancy-induced hypertension resulting from RUPP does not elicit manifestations of metabolic syndrome in late-gestation rat dams.
authors.affiliation: Department of Physiology and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, MS 39216-4505, USA.
authors.forename: Jeffrey
authors.initials: J
authors.lastname: Gilbert
authors.forename: Matt
authors.initials: M
authors.lastname: Dukes
authors.forename: Babbette
authors.initials: B
authors.lastname: LaMarca
authors.forename: Kathy
authors.initials: K
authors.lastname: Cockrell
authors.forename: Sara
authors.initials: S
authors.lastname: Babcock
authors.forename: Joey
authors.initials: J
authors.lastname: Granger
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D004195:Disease Models, Animal; D005260:Female; D005947:Glucose / Q000378:metabolism*; D005951:Glucose Tolerance Test / Q000379:methods; D007328:Insulin / Q000097:blood; D024821:Metabolic Syndrome / Q000378:metabolism / Q000503:physiopathology; D010477:Perfusion; D011225:Pre-Eclampsia / Q000378:metabolism* / Q000503:physiopathology; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D052243:Resistin / Q000097:blood; D014280:Triglycerides / Q000097:blood; D014599:Uterus / Q000098:blood supply* / Q000502:physiology
chemical_list: D007328:Insulin; D052243:Resistin; D014280:Triglycerides; D005947:Glucose