During pregnancy parathyroid hormone-related protein (PTHrP) is one of many growth factors that play important roles to promote fetal growth and development including stimulating placental calcium transport. Angiotensin II, acting through the AT1_a, receptor is also known to promote placental growth. We examined the effects of bilateral uterine artery and vein ligation (Restricted), which mimics placental insufficiency in humans, on growth, intrauterine PTHrP, placental AT1_a and pup calcium. Growth restriction was surgically induced on day 18 of pregnancy in the Wistar Kyoto female rat by uterine vessel ligation. Uteroplacental insufficiency reduced fetal body weight by 15% and litter size (P<0.001) compared to Control with no effect on placental weight or amniotic fluid volume. Uteroplacental insufficiency reduced placental PTHrP content by 46% with increases in PTHrP (by 2.6 fold), PTH/PTHrP receptor (by 11.6 fold) and AT1_a (by 1.7 fold) relative mRNA in placenta following Restriction compared to Control (P<0.05). There were no alterations in uterine PTHrP and PTH/PTHrP receptor mRNA expression. Maternal and fetal plasma PTHrP and calcium concentrations were unchanged. Although fetal total body calcium was not altered, placental restriction altered perinatal calcium homeostasis as evidenced by lower pup total body calcium after birth (P<0.05). The increased uterine and amniotic fluid PTHrP (P<0.05) may be an attempt to compensate for the induced impaired placental function. The present study demonstrates that uteroplacental insufficiency alters intrauterine PTHrP, placental AT1_a expression and perinatal calcium in association with a reduction in fetal growth. Uteroplacental insufficiency may provide an important model for exploring the early origins of adult diseases.