Preeclampsia is a gestational disorder affecting 4-8% of all pregnancies.  It is characterized by mid-gestational onset of hypertension, proteinuria, and multi-organ system failure leading to increased maternal and fetal morbidity and mortality.  Currently, there are no practical screening tests or treatments for preeclampsia.  Indeed, the only “cure” for preeclampsia has been and remains to be the delivery of the fetus and placenta.  Recently, our group has discovered that arginine vasopressin (AVP) secretion is elevated as early as six weeks gestation in women who will go on to develop preeclampsia later during their pregnancy. We found that AVP infusion throughout pregnancy in mice leads to phenotypes of preeclampsia, including hypertension, proteinuria, fetal growth restriction, and renal glomerular endotheliosis.  To understand the mechanism by which AVP induces symptoms of preeclampsia, we used selective antagonists to characterize the AVP receptor(s) responsible for individual phenotypes. We found that V1b receptor inhibition with nelivaptan prevented the effect of AVP to induce fetal growth restriction in pregnant mice.  We also found that the infusion of nelivaptan had no effect on proteinuria induced by AVP in pregnant mice. These results support the concept that the V1b receptor for AVP is mechanistically involved in the fetal, but not maternal, phenotypes of preeclampsia.  We anticipate that these studies will ultimately lead to the development of novel pharmaceutical approaches for individual symptoms of preeclampsia.