Elevated leptin (lep) in pregnant women strongly associates with preeclampsia (PE), a hypertensive pregnancy disorder. Our lab established a mid-late gestation lep-infusion model of PE, which induces endothelial dysfunction, hypertension and fetal growth restriction (FGR); deletion of endothelial mineralocorticoid receptors (MR) ablated these PE characteristics in pregnant mice. Whether pharmacological MR antagonism ablates lep-induced PE, however, is unknown. We hypothesized that MR antagonism (eplerenone) ablates lep-induced PE characteristics in pregnant mice. We infused pregnant BALB/c mice with leptin (lep, 0.9mg/kg/day) or saline (sham) via osmotic minipump alongside eplerenone (Eplr, 200mg/kg/day) or vehicle in drinking water from gestation day (GD)11-18. We measured vascular function via wire myography of 2 nd order mesenteric vessels and pup/placental weights on GD18 (n=5-7). We implanted radiotelemeters in separate mice (n=1-3) prior to mating and measured mean arterial pressure (BP) from GD11-18. Pre-pregnancy BP did not differ between treatment groups. Preliminary data indicates lep increased BP compared to sham from GD11-18 (112.7±4.5 lep vs 89.4 sham mmHg,) and Eplr decreased BP in lep pregnant mice (97.2±7.2 lep+Eplr mmHg, P=0.09 vs lep student’s t-test). Vascular relaxation to endothelial-dependent acetylcholine (ACh) decreased in lep+vehicle compared to sham+vehicle (*P<0.05, 2-Way ANOVA w/ RM). Eplr+lep restored ACh-mediated vascular relaxation (*P<0.05 vs lep+vehicle). LNAME pre-incubation did not ablate differences in ACh-mediated relaxation between lep+vehicle and lep+eplr (P>0.05) indicating that Eplr restored a non-NO mechanism to improve endothelial function. Lep as a variable decreased pup weight in both vehicle and Eplr pregnant mice, however, Eplr did not increase pup weight in either vehicle or lep mice (0.74±0.01sham+veh, 0.71±0.01 lep+veh, 0.70±0.01 sham+eplr, 0.67±0.01 lep+eplr (g), *P<0.05, 2-Way ANOVA). Collectively these data indicate that Eplr improves lep-induced endothelial dysfunction and hypertension, but may not prevent FGR when given from GD11-18. Therefore, further studies will determine whether MR antagonism promises therapeutic potential in lep-induced PE.