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


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

Postgraduate Training


 Duke University Health System


Duke University Health System


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.