Tribute to Emory Cardiology

The role of angiotensin II in hypertension is a major focus of research in the Cardiology Division at Emory. This work largely stems from Dr. Alexander’s seminal observations regarding the effect of angiotensin II on vascular smooth muscle. Dr. Alexander began this research in the 1970s and has contributed importantly to our understanding of the molecular mechanisms of angiotensin II signaling. Dr. Kathy Griendling has recently shown that a major effect of angiotensin II is activation of vascular smooth muscle production of reactive oxygen species. Work from her laboratory has shown that this occurs via activation of a p22phox based-NADH/NADPH-dependent oxidase. Importantly, generation of reactive oxygen species by this oxidase is critical for the hypertrophic response to angiotensin II. Dr. David Harrison’s laboratory, in collaboration with Dr. Griendling, has shown that this oxidase is activated in-vivo as a result of angiotensin II-induced hypertension. Dr. Robert Taylor’s group has investigated the inflammatory response induced by angiotensin II mediated hypertension, and has demonstrated its dependence on MCP-1. Mice deficient in the MCP-1 receptor do not develop this inflammatory response and importantly do not have vascular hypertrophy. His laboratory is also interested in the mechanical effect of hypertension on endothelial and vascular smooth muscle cells. Thus, research in the Emory Cardiology Division has developed the novel concept that hypertension imposes an oxidative stress on the vasculature. This concept is now widely accepted, and has opened a new direction in hypertension research. Note: This is the unofficial web tribute to Emory Cardiology that has been put together as a token of gratitude for the exceptional training that Dr. Chung had received as a cardiology fellow (1997-2001). Copyright © 1998-2007 Andrew B. Chung, M.D., Ph.D. All rights reserved. Date of last update: 11/20/2008