Prenatal vitamin D supplementation reduces blood pressure and improves placental angiogenesis in an animal model of preeclampsia.

Abstract

Preeclampsia (PE), a pregnancy complication, is characterized by abnormal placental angiogenesis. The current study examines the effect of vitamin D deficiency/supplementation on pregnancy outcome and placental angiogenesis using an animal model of PE. Pregnant Wistar rats were divided into four groups: Control; PE; Vitamin D deficient with PE (VDD-PE) and Vitamin D supplemented with PE (VDS-PE). PE was induced by administering l-nitroarginine methyl ester (l-NAME) at the dose of 50 mg per kg body weight per day from day 14 to day 19 gestation in all the 4 groups. During the pre-pregnancy and pregnancy period, the rats from the Control and PE groups were fed a control diet, the VDD-PE group received a vitamin D deficient diet and the VDS-PE group received a vitamin D supplemented diet. Dams were sacrificed at d20 of gestation. l-NAME administration increased systolic as well as diastolic blood pressure in both PE and VDD-PE groups as compared to the control (p < 0.01). Vitamin D supplementation was beneficial in reducing the blood pressure. Vitamin D deficiency also lowered the placental protein levels of pro-angiogenic proteins VEGF and Flt-1 (p < 0.05 and p < 0.01, respectively), while the levels of these proteins in the VDS-PE group were similar to those in the control group. Vitamin D status did not influence the levels of PlGF and Hif1α. A low dose vitamin D supplementation given from pre-pregnancy and throughout pregnancy was beneficial in reducing the blood pressure and normalizing the placental levels of VEGF and Flt-1. This has implications for reducing the severity of preeclampsia.