Altered fetal growth patterns, i.e. reduced growth in utero (intrauterine growth restriction, IUGR) are associated with perinatal morbidity as well as adverse consequences in adult life, e.g. cardiovascular disease. A prevailing hypothesis regarding the pathogenesis of reduced growth in utero is the “ischemic model” where abnormal placental bed vascular pathology with reduced nutrient and oxygen delivery to the intervillus space as a result of diminished placental perfusion contributes to suboptimal fetal growth in the second half of pregnancy. Amino acids are an important nutrient during fetal development and their concentration and placental transport are significantly lower in growth-restricted infants. Recent studies indicate that a variety of signals such as adenosine are produced in response to hypoxia in tissues and are higher in women with preeclampsia and growth-restricted infants. However, to date there is little information about the role of adenosine in pregnancy and the placenta. Therefore, the focus of this proposal is to investigate the effect and mechanism of the hypoxia-inducible signal adenosine on placental development and placental amino acid transport.