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  • Research Summary for Joey Granger, PhD

    The renal-body fluid feedback concept for long-term arterial pressure control has been supported by numerous experimental studies and integrative analysis of the circulatory, renal, and neurohormonal systems. Several lines of evidence also support an important role for the kidneys in hypertension. Recent studies from our laboratory have focused on the physiological mechanisms whereby endothelial derived factors alter renal function and lead to long-term alterations in the regulation of arterial pressure and hypertension. A major goal of our laboratory is to examine the role of endothelin, nitric oxide, thromboxane and other humoral factors in mediating the reduction in renal-pressure natriuresis in a specific form of hypertension associated with endothelial dysfunction--pregnancy-induced hypertension (PIH).

    Pregnancy-induced hypertension is estimated to affect 5-10% of all pregnancies in the U.S. Despite being the leading cause of maternal death and a major contributor of maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of pregnancy-induced hypertension are unclear. Hypertension associated with preeclampsia develops during pregnancy and remits after delivery implicating the placenta as a central culprit in the disease.

    The initiating event in PIH has been postulated to involve reduced placental perfusion which leads to widespread dysfunction of the maternal vascular endothelium by mechanisms that remain to be determined.

     Our working hypothesis is that a reduction in uteroplacental perfusion pressure causes hypertension by reducing renal-pressure natriuresis. The reduction in pressure natriuresis occurs as a result of placental factor(s) causing endothelial cell dysfunction that lead to enhanced formation of vasoconstrictors (endothelin and thromboxane) and decreased formation of vasodilators (nitric oxide and prostacyclin). These endothelial abnormalities reduce renal plasma flow and glomerular filtration rate or enhanced tubular reabsorption, thereby decreasing renal sodium excretory function.

    To test this hypothesis, arterial pressure, renal, hormonal, and endothelial function will be examined in a conscious, chronically-instrumented rat model of chronic PIH produced by long-term reductions in uterine perfusion pressure (RUPP). Preliminary data in this model indicate that the hypertension produced by decreased blood flow to the uteroplacental unit is associated with proteinuria, significant reductions in renal plasma flow and GFR, a hypertensive shift in the pressure natriuresis relationship, and endothelial dysfunction.