Sodium Sensitive Hypertension
We are exploring how WNK kinase signal transduction pathways regulate the thiazide sensitive sodium-chloride cotransporter (NCC) in the Kidney. NCC plays an important role in sodium balance and blood pressure control, and is the molecular target of first line antihypertensive drugs, the thiazide diuretics. Inherited mutations, environmental stresses, and low dietary potassium over activate the WNK kinases signaling cascade, causing aberrant activation of NCC, and sodium-sensitive hypertension. Current investigation builds on our successful efforts to create and study new mouse models of the signaling pathway. Our focus is on identifying and studying the molecular factors that adjust or turn off the WNK signaling pathway. Funded by the National Institutes of Health, National Institute of Diabetes, Digestive and Kidney Diseases DK093501 as a Multi-PI grant with Eric Delpire at Vanderbilt.