Maturation of fetal tissues requires glucocorticoid binding to the glucocorticoid receptor (GR). GR is also expressed in the placenta though a functional role in placenta is not established. We hypothesised that glucocorticoids act via GR to modify placental function to meet fetal demand, particularly in late gestation. Here, we tested the effect of GR deletion upon placental growth and hemodynamic function. Heterozygous GR mice, with C57BL/6J background, were time-mated to produce litters of WT, Het and GRKO fetuses. The morning of vaginal plug was designated E0.5. In vivo pulsed-wave Doppler ultrasound scanning was conducted at E14.5 or E17.5 to measure umbilical artery (UA) blood flow and fetal heart function. Immediately after scanning, tissues were collected. Data were analysed by two-way ANOVA with post-hoc Bonferroni’s test. Global GR ablation did not alter fetal wet weight at E14.5 or E17.5, although placental wet weight was increased at E17.5 (p=0.003). At E14.5, UA blood flow was largely unchanged. Conversely, at E17.5, GRKO exhibited reduced UA systolic/diastolic ratio (p=0.002) and diastolic flow was detectable in only 38% of GRKO compared to 83% of WT. UA resistance index was increased in GRKO (p=0.0004). Moreover, whilst reversed end-diastolic flow (REDF) was undetectable in WT by E17.5, it persisted in GRKO. Minimal effects were seen on fetal heart function. GR ablation increased placental weight in late gestation, when endogenous glucocorticoid levels peak, perhaps reflecting the removal of normal growth inhibitory effects of glucocorticoids. Further, the compromised UA blood flow associated with persistence of REDF and high resistance index in GRKO indicates a functionally immature placenta at E17.5. Interestingly, despite impaired placental blood flow, fetal wet weight was maintained in GRKO. This is consistent with our previous report of fetal oedema in GRKO. Investigation is underway to determine how absent GR signalling affects placental morphology and fetal-placental interactions.