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(Hypertension. 2006;47:515.)
© 2006 American Heart Association, Inc.
Corcoran Lecture |
From the Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston Salem, NC.
Correspondence to Carlos M Ferrario, Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston Salem, NC 27157. E-mail cferrari{at}wfubmc.edu
This lecture summarizes the chronology and rationale that led to the discovery of angiotensin-(1-7) as a hormone that, in its own right, opposes the vasoconstrictor and proliferative actions of angiotensin II. The work discussed here additionally analyzes the newest findings on angiotensin-converting enzyme 2, the angiotensin-converting enzyme homologue that efficiently hydrolyzes angiotensin II into angiotensin-(1-7). Both components of this system may significantly influence our future perspective of the role of the reninangiotensin system, not just in terms of its role in the regulation of cardiovascular and renal function but, moreover, as regulators of a vast array of disease processes in which inflammation and immune mechanisms play a role.
Key Words: hypertension receptors, angiotensin angiotensin converting enzyme angiotensin II
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