Associate Professor Office: G306(601) 984-1629
My laboratory is interested in determining factors that lead to kidney disease during hypertension (high blood pressure) and identifying new targets for the treatment of these diseases. Previous work has shown that production of nitric oxide (NO) is decreased in chronic kidney disease, and this contributes to cardiovascular risk and to further progression of kidney damage. Therefore, interventions that can restore NO production are likely to reduce the cardiovascular complications of CKD as well as slow the rate of progression of renal injury.Our current work is focused on two main projects. The goal of our first project is to test the therapeutic potential of relaxin in rodent models of kidney disease, specifically focusing on the effects of relaxin on the renal endothelin-NO pathway. Relaxin, a hormone that is increased in normal pregnancy, has been shown to cause vasodilation and increase renal blood flow via increased NO production. In addition, relaxin is also anti-fibrotic and may therefore improve kidney structure in disease states. In our second project, we have begun to examine the initiating causes of preeclampsia and the mechanisms by which the development of preeclampsia alters glomerular structure and function during pregnancy.Our laboratory has recently characterized the Dahl Salt Sensitive rat (on a 0.3% salt diet) as a model of preeclampsia that closely mimics the human disease. In addition to understanding the disease in pregnancy itself, we will also use this model to determine the effects of preeclampsia on the later development of cardio-renal disease in both the mother and the offspring. We use whole animal and molecular approaches including acute and chronic measurements of blood pressure and renal function and measures of protein abundance and activity.