Graduate Studies Faculty

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David H. Ellison, MD

Professor of Medicine
Head, Division of Nephrology & Hypertension
Admin Unit: SOM-DOM Nephrology & Hypertension
Phone: 503-494-8490
Fax: 503-494-5330
Mail Code: PP262
Physiology & Pharmacology
Program in Molecular & Cellular Biosciences
Research Interests:
hypertension, genetic basis of human blood pressure control, translational medicine, ion transport, cardiovascular disease, physiology, thiazide-sensitive Na-Cl cotransporter, edema, heart failure, signal transduction, aldosterone, steroid hormones, Gitelman's syndrome, familial hyperkalemic hypertension, genetic kidney disease » Click here for more about Dr. Ellison's research » PubMed Listing
Preceptor Rotations
Dr. Ellison has not indicated availability for preceptor rotations at this time.
Faculty Mentorship
Dr. Ellison has not indicated availability as a mentor at this time.

      Our laboratory conducts basic and translational experiments designed to elucidate the mechanisms of human hypertension and to improve its treatment. Hypertension affects 50 million Americans, making it the country's most common disease.  Although treatments are available, less than 50% of patients who have the disease are adequately controlled.  Hypertension has a strong genetic component, but the nature of the genes involved in most hypertension remains unknown.  We have studied genes that when mutated cause either hypertension, or its converse, low blood presure.  We have identified a unique and previously unrecognized kinase pathway, the WNK kinases, that appears to be a molecular rheostat, which can switch the kidney from a potassium secretory organ to a sodium retentive one.  When this pathway is genetically disturbed, hypertension results.
     Our studies have utilized heterologous expression of normal and mutant proteins in Xenopus oocytes, evaluation of trafficking mechanisms in mammalian cultured cells, development of transgenic models systems in mice, and dietary manipulation of wild type and transgenic animals.  Recently, we have extended our findings from the laboratory to human studies and are developing methods to more accurately diagnose salt wasting diseases, such as Gitelman's syndrome.  We also conduct work using animals models of human physiology and disease.  We have recently described how immunosuppressive drugs can lead to hypertension and hyperkalemia and are extending this work to look for novel approaches to immune therapy devoid of such side effects.  Our work holds the potential to develop a personalized approach to hypertension, based on its pathogenesis in individuals; to this end, we are now exploring the possibility of identifying hypertensive individuals likely to manifest dysfunction of specific regulatory pathways.  Such identification would permit targeted and more effective dietary or drug approaches to essential hypertension.