Jeremy Sandgren, graduate student in Dr. Grobe's laboratory, was awarded a Predoctoral Fellowship from the American Heart Association's Midwest Affiliate for his project entitled "Vascular mechanisms of vasopressin action in a novel mouse model of preeclampsia."  Preeclampsia affects 4-8% of all pregnancies and is characterized by mid-gestational maternal hypertension, proteinuria, multi-system organ failure, and can lead to maternal and fetal death. At this time, the only cure for preeclampsia is fetal and placental delivery, which is often premature and therefore a risk for both the mother and child. Recently, our group discovered that maternal plasma copeptin, a marker for arginine vasopressin (AVP) secretion, is elevated throughout pregnancies that eventually develop preeclampsia starting as early as the 6th week of gestation. Additionally, we found that AVP infusion throughout mouse gestation is sufficient to induce symptoms of preeclampsia, including hypertension, proteinuria, fetal growth restriction, and renal glomerular endotheliosis. Our long-term goal is to understand the role of AVP in preeclampsia. However, in this proposal, we are specifically interested in the effects of AVP on the uterine artery, which, like AVP secretion, is dysfunctional early in pregnancy before the onset of preeclampsia.

John Reho, Ph.D., Postdoctoral Research Scholar in Dr. Rahmouni's laboratory, was awarded a Postdoctoral Fellowship from the American Heart Association's Midwest Affiliate for his project entitled "mTORC1 as a Novel Regulator of Vascular Function in Obesity."  Obesity-induced hypertension is associated with vascular endothelial dysfunction. As a postdoc in the Rahmouni lab, we have focused on the mammalian target of rapamycin complex 1 (mTORC1) as a novel signaling pathway in the regulation of the cardiovascular system. Specifically, the activation of the central mTORC1 triggered a significant increase in arterial pressure. In this proposal, we are testing the hypothesis that dysregulation of mTORC1 signaling is involved in the vascular endothelial dysfunction associated with obesity in mice. We have 1) demonstrated vascular dysregulation of the mTORC1 pathway in the pathology associated with obesity in both mice and humans 2) demonstrated that direct activation of the mTORC1 pathway results in endothelial but not smooth muscle dysfunction; a hallmark of the vascular pathology associated with obesity-induced hypertension.