Effects of reduced uterine perfusion pressure on blood pressure and metabolic factors in pregnant rats.
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.
Gilbert
Jeffrey
J
Department of Physiology and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, MS 39216-4505, USA.
Dukes
Matt
M
LaMarca
Babbette
B
Cockrell
Kathy
K
Babcock
Sara
S
Granger
Joey
J
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
D007328:Insulin; D052243:Resistin; D014280:Triglycerides; D005947:Glucose