These responses in vasoactivity are interesting because fetal growth was reduced during the nutrient restriction, in association with the increased placental vasoconstrictor response, whereas fetal size was normal in the re-fed dams late in gestation, when the placental vasoconstrictor response was blunted. In uterine arteries of rats in which placental perfusion is reduced experimentally, the vasoconstrictor response is enhanced, whereas endothelium-dependent vasorelaxation is reduced (Anderson et al. 2005). Interestingly, in humans the vasoconstrictor response of placental arteries to U46619, a thromboxane mimetic, was reduced in pregnancies exhibiting pre-eclampsia or intrauterine fetal growth restriction (Wareing & Baker, 2004). Thus, although the responses are complex, placental vasoactivity seems to be altered, and vasoactive factors are therefore logical therapeutic targets in compromised pregnancies.