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

MD - Oklahoma State Univ
BS, Oklahoma State University, Stillwater, Oklahoma

Postgraduate Training

Internship

 Duke University Health System

Residency

Duke University Health System

Fellowship

Duke University Health System

University of Iowa Healthcare

Board and Certifications
  • Cardiovascular Disease - American Board of Internal Medicine, 1979
  • Internal Medicine - American Board of Internal Medicine, 1977

Clinical Interest

Areas of Expertise

  • Cardiovascular Medicine
  • General Cardiology
  • Heart and Vascular
  • Interventional Cardiology and Peripheral Vascular Disease
Research Keywords
Vascular Biology;Hypertension
Research Description

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.