Women of advanced maternal age (AMA; >35 years) are an increasingly prevalent obstetric population and a high risk group for fetal growth restriction (FGR) and stillbirth. Adequate perfusion of the utero-placental unit and blood flow to the fetus are essential for a healthy pregnancy; under-perfusion of the placenta is associated with FGR, which is in turn associated with stillbirth. It is known that ageing affects the cardiovascular system, including a loss of vascular responsiveness and vascular wall thickening. Studies have found increased vascular thickness and decreased uterine artery remodelling in aged pregnant mice, in conjunction with reduced fetal weight and increased infant death; however the effect of AMA on utero-placental vascular function has not yet been investigated in human pregnancies. We hypothesised that maternal ageing alters placental and myometrial arteries function, leading to increased susceptibility to poor outcomes in these pregnancies. Tissue was collected from pregnant women aged 20-30 (control), 35-39 and ≥40 years delivering at St Mary’s Hospital, Manchester. Placentas (n=15/group) were collected following normal vaginal delivery or caesarean section. Myometrial samples were collected following caesarean section (n=4/group). Placental chorionic plate and myometrial resistance arteries (100-500µm diameter) were dissected. Wire myography was used to assess responses to the vasoconstrictor U46619 (thromboxane mimetic; 10-9 to 10-5.7 M) and vasodilators sodium nitroprusside (SNP; 10-11 to 10-6 M) and bradykinin (BK; 10-10 to 10-5 M) (myometrium only). Significance is defined as p<0.05 after 2-Way ANOVA with post hoc tests. There was no effect of AMA on placental artery constriction in response to U46619. Pre-constricted placental arteries from 35-39 and ≥40 year old mothers showed increased relaxation to SNP compared to controls. Myometrial vessels from ≥35 year old mothers showed decreased constriction to U46619. There was no consistent effect of vasodilators on myometrial vessels. Both placental and chorionic plate arteries from older women exhibit altered vascular reactivity compared with younger mothers. As SNP acts as an NO donor, the increased response to SNP in placental arteries from older mothers may be due to increased sensitivity to NO as a result of an age related decrease in endogenous NO. AMA seems to affect placental vascular function despite the placenta being fetal in origin and therefore a ‘young’ organ. Decreased constriction of myometrial vessels from AMA mothers may alter blood flow to the uterus and could be due to age related loss in baroreceptor sensitivity or circulating maternal factors associated with ageing. Altered vascular control over blood flow to the placenta and baby may contribute to the increase in poor pregnancy outcomes in AMA pregnancies.