Abstract
Vitamin D (VD) deficiency is associated with preeclampsia (PE) and has been shown to regulate immune responses. We tested the hypothesis that VD2 and VD3 treatment ameliorates hypertension and or immune activation in our Reduced Uterine Perfusion Pressure (RUPP) model of PE. RUPP was performed on gestation day 14 (GD14) with 50uM VD2 or VD3 treatment on GD14-18. Sacrifice and MAP measurement were on GD19. MAP in RUPP rats was 122±2.3 compared to 104.2±2.4 mmHg in NP rats (p<0.05). Supplementation with either VD2 or VD3 lowered MAP to 117.6±3.9 and 114.3±2.9 mmHg. CD4+ T cells increased from 2.8±1.0 in NP to 8.5±1.5% in RUPP (p<0.05) and decreased to 1.2±0.4 % with VD2 and 4.6±3.7 % with VD3. AT1-AA, measured via cardiomyocyte chronotropic responses, were 19.5±0.4 beats/min in RUPP rats and decreased to 15.4±0.7 with VD3 (p<0.05), and further to 8.3±0.5 with VD2 (p<0.05). Circulating B cells increased in RUPP rats compared to NP (5.5±3.7% to 9.0±5.8%) while VD2 and VD3 had no effect (11.6±3.1%, 6.8±4.2 %) indicating B cell activation rather than population was decreased in VD treated RUPP rats. These data indicate that VD reduced MAP and inflammation in a rat model of PE, implying a role for VD in the pathogenesis of PE.
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