Effects of reduced uterine perfusion pressure on blood pressure and metabolic factors in the pregnant rat

Abstract

Placental ischemia is thought to be the initiating factor in preeclampsia. Although elements of the metabolic syndrome are often present in preeclamptic pregnancies, it remains unclear whether these metabolic aberrations presage or result from placental ischemia. This purpose of this study was to examine metabolic factors in response to chronic reductions in uterine perfusion pressure (RUPP). We measured arterial pressure, fasting plasma concentrations of triglycerides (TG), glucose, resistin, insulin and glucose tolerance at day 19 of gestation. Mean arterial pressure increased (130 ± 2.1 vs. 100 ± 4.3 mm Hg) and fetal weight decreased (1.93 ± 0.08 vs. 2.19 ± 0.06 g) in RUPP rats compared to normal pregnant (NP) rats. Maternal fasting glucose (4.2 ± 0.3 vs. 3.1 ± 0.4 mmol/l; P = 0.05) tended to increase in RUPP compared to NP rats. Serum TGs (2.62 ± 0.29 vs. 2.45 ± 0.51 mmol/l), insulin (9.9 ± 0.7 vs. 8.5 ± 0.7 μU/ml), resistin (46.25 ± 4.19 vs. 49.71 ± 4.01 pg/ml), and glucose area under the curve (650 ± 35 vs. 570 ± 34 mmol/min/l) were not different between the RUPP and NP rats. Although these findings do not discount the hypothesis that pre-existing symptoms of the metabolic syndrome may contribute to the onset of preeclampsia in women, these data clearly show that pregnancy induced hypertension resulting from RUPP does not elicit manifestations of the metabolic syndrome in late gestation rats.