Preeclampsia, a pregnancy-specific condition characterized by hypertension and proteinuria, affects 5-8% of pregnancies in the US. Cerebrovascular events are implicated in ~40% of preeclampsia/eclampsia-related deaths and neurological symptoms are common in preeclamptic patients. Despite strong clinical evidence for cerebrovascular involvement, the etiology of preeclampsia-induced cerebrovascular abnormalities is poorly understood.
Our laboratory demonstrated that placental ischemia, induced by reducing uterine perfusion pressure (RUPP), produces similar symptoms as preeclamptic patients, including cerebrovascular abnormalities. However, the link between placental ischemia and the resulting cerebrovascular abnormalities is not known.
Therefore, our objectives are:
1) To determine whether placental ischemia leads to reduced cerebral blood flow autoregulation and increased blood-brain barrier permeability
2) To identify the key molecules, altered in preeclampsia (TNFα, βENaC, sFlt-1, AT1-aa), that contribute to impaired cerebrovascular function in placental ischemic rats
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