One of the common factors apparent in several animal models of prenatal stress is impairment of uteroplacental vascular function. This can lead to a reduction in the delivery of oxygen and nutrients to the developing fetus, resulting in reduced fetal growth and subsequently long-term programming of disease. Whilst we still do not fully understand the mechanisms underpinning impaired uteroplacental function in compromised pregnancies, interventions aimed at enhancing nitric oxide bioavailability remain a key area of interest in obstetric research. Dietary nitrate (abundant in green leafy vegetables and beetroot) is an important modulator of cardiovascular function in non-pregnant humans and animals. Treatment with dietary nitrate, providing an exogenous source of nitric oxide (NO) and other bioactive nitrogen oxides, can improve blood flow, vascular function and reduce damage caused by ischemia-reperfusion injury. We have shown that maternal dietary nitrate supplementation, via beetroot juice, improves ex vivo uterine artery function in a model of fetal growth restriction associated with vascular dysfunction, the endothelial nitric oxide synthase knockout (eNOS-/-) mouse. This improvement in vascular function was associated with elevated plasma nitrate and nitrite (NOx) concentrations. Nitrate-depleted beetroot juice, which failed to elevate plasma NOx levels, did not alter maternal vascular function. Our ongoing studies aim to determine the mechanisms underlying the beneficial effects of dietary nitrate supplementation on vascular function, using both animal models and human uteroplacental tissue. In parallel, we are now also investigating the effects of a short-term dietary nitrate supplementation on cardiovascular function and uteroplacental blood flow in pregnant women. Together, these studies aim to develop an acceptable and efficacious dietary intervention that can improve both maternal and fetal outcomes in compromised pregnancies.