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(Circulation Research. 2004;94:1.)
© 2004 American Heart Association, Inc.

Editorials

ACE, ACE Inhibitors, and Other JNK

Michael J. Ryan, Curt D. Sigmund

From the Department of Medicine, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, Iowa.

Correspondence to Curt D. Sigmund, PhD, Professor, Department of Internal Medicine, 3181 MERF, University of Iowa, Department of Internal Medicine, Iowa City, IA 52242. E-mail Curt-Sigmund@uiowa.edu

Key Words: intracellular signaling • c-Jun N-terminal kinase • c-Jun • angiotensin-converting enzyme • angiotensin-converting enzyme inhibitors

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The renin-angiotensin system (RAS) plays a pivotal role in the regulation of blood pressure, volume homeostasis, vascular function, and cell growth. In what is considered the classic RAS, renin is released from juxtaglomerular cells of the kidney into the circulation where it converts angiotensinogen from the liver to angiotensin I. Angiotensin I is subsequently hydrolyzed by a peptidyl dipeptidase, angiotensin-converting enzyme (ACE), from the lung to form angiotensin II. Investigators have been cognizant of renin for more than a century after its initial discovery in 1898 by Tigerstedt and Bergman (see review¹). However, it was not until the middle of the 20th century that the remaining components of RAS were purified and identified by Skeggs and colleagues. These included angiotensinogen, angiotensin I, angiotensin II, and ACE, which at the time was termed "hypertensin-converting enzyme" (see review¹). Since that time, many components of the RAS, especially ACE, have received considerable attention as a focal point for researchers interested in better understanding the regulation of the cardiovascular system.

Considering the rapid progress in understanding the molecular physiology of RAS and its many complexities, it should not be surprising that details would continue to emerge. It is unexpected, however, that after 100 years of research major new concepts would surface requiring scientists and clinicians to rethink the system and its role in cardiovascular regulation. Even more astounding is that over the span of 3 years, two major conceptual changes would have to be considered regarding ACE. The first surprise occurred in . . . [Full Text of this Article]

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