David G. Harrison, MD, FACC, FAHA
Office Address:
536 RRB, Nashville, TN 37232
Director, Division of Clinical Pharmacology
Professor, Department of Medicine
Betty and Jack Bailey Chair in Cardiology
Professor, Department of Pharmacology
Professor, Department of Molecular Physiology & Biophysics
Education
Relevant Links
Postgraduate Training
Duke University Health System
Duke University Health System
Duke University Health System
University of Iowa Healthcare
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- Cardiovascular Disease - American Board of Internal Medicine, 1979 ⇥
- Internal Medicine - American Board of Internal Medicine, 1977
Clinical Interest
Areas of Expertise
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- Cardiovascular Medicine ⇥
- General Cardiology ⇥
- Heart and Vascular ⇥
- Interventional Cardiology and Peripheral Vascular Disease
Our laboratory has been focused on understanding how inflammation, and in particular, the adaptive immune response contributes to hypertension. Several years ago, we found that T cells are essential for the development of hypertension. We have shown that various hypertensive stimuli, including angiotensin II, norepinephrine and DOCA-salt cause activation of T cells and leads to their accumulation in the perivascular fat and kidneys. Our data indicate that T cell-derived cytokines such as IL-17 and TNF-a enhance vasoconstriction and sodium retention, leading to the hypertensive phenotype. Central signals derived from the circumventricular organs contribute to T cell activation, and manipulation of signals from this region affect T cell activation and the eventual elevation in blood pressure caused by angiotensin II. We are attempting to understand mechanisms involved in T cell activation in response to hypertensive stimuli. We have recently shown that gamma-ketoaldehydes, or isoketals adduct to proteins in hypertensive mice and humans, and that these are immunogenic. These modified proteins seem to act as 'auto-antigens' that promote dendritic cell and ultimately T cell activation in hypertension.