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(Circulation. 2002;105:1523.)
© 2002 American Heart Association, Inc.

Editorials

Does Angiotensin-(1–7) Contribute to Cardiac Adaptation and Preservation of Endothelial Function in Heart Failure?

Carlos M. Ferrario, MD

From the Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, NC.

Correspondence to Carlos M. Ferrario, MD, The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Winston-Salem, NC 27157. E-mail cferrari@wfubmc.edu

Key Words: Editorials • angiotensin • endothelium • heart failure

In the late 1890s, the Finish physiologist Robert Tigerstedt made the fundamental observation that aqueous extracts of kidneys caused a prolonged rise in the blood pressure of anesthetized animals.^1a The clinical significance of this finding remained unappreciated for more than 30 years until Hessel, a disciple of Volhart, provided evidence for the participation of renin in the production of what they termed "white hypertension." Even in our current setting, roughly a century later, application of the observations made by the Scandinavian investigators continues to provide an illuminating example of the complexity of the scientific endeavors that make medical science an art of unrelenting inquiry and often of late recognition. In fact, continuing efforts to understand the biological actions of the renin-angiotensin system have led to impressive clinical applications that are reflected in current therapeutic approaches to the treatment of high blood pressure and the prevention of stroke, congestive heart failure, and end-stage renal disease. The introduction of angiotensin converting enzyme (ACE) inhibitors expanded knowledge of the mechanisms through which the renin-angiotensin aldosterone system acts as a mediator of cardiovascular pathology and became the basis for the later development of orally active angiotensin II antagonists. Although the majority of clinical endeavors and research efforts continues to concentrate on pharmacological strategies aimed at interrupting the actions of angiotensin II (Ang II), emerging concepts suggest that the important homeostatic functions regulated by the renin-angiotensin system may be influenced, in part, by the actions of other angiotensin peptides derived from either angiotensin I (Ang . . . [Full Text of this Article]

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