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Circulation Research. 2008;102:628-629
doi: 10.1161/CIRCRESAHA.108.173781
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(Circulation Research. 2008;102:628.)
© 2008 American Heart Association, Inc.


Editorials

Angiotensin-Converting Enzyme 2

A New Player in Central Sympathetic Regulation?

Irving H. Zucker

From the Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha.

Correspondence to Irving H. Zucker, PhD, Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, 985850 Nebraska Medical Center, Omaha, NE 68198-5850. E-mail izucker@unmc.edu



See related article, pages 729–736


Key Words: adrenergic regulation • angiotensin II • ACE 2


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

There is a "new kid on the block" in the control of the renin-angiotensin system (RAS). The discovery of angiotensin (Ang)-converting enzyme (ACE)2, a catabolic enzyme, that cleaves the octapeptide, Ang II into a septapeptide, Ang-(1-7),1,2 has opened up new vistas in the way we think about the regulation and biological effects of Ang II. ACE 2 was originally discovered in yeast3 as a gene product that codes for a protein that is a homolog of the more widely known protease ACE. ACE2 cleaves the C-terminal amino acid from Ang II and other peptides. For many years, the work of Ferrario and Chappel4 provided evidence that Ang-(1-7) operated in the central nervous system, as well as in the peripheral circulation to produce effects that were, in general, opposite to that of Ang II. Recently, the discovery that Ang-(1-7) binds to a specific membrane receptor, the mas receptor,5–7 suggests that this metabolite may play a regulatory role in cell signaling and organ function. Clearly, the balance between the classic ACE and ACE2 will determine the physiological effect of activation of the RAS. Furthermore, the potential for therapeutic targeting of ACE2 and its role in the pathogenesis of various diseases such as hypertension and heart failure is intriguing.

To further understand the potential for ACE 2 in the brain to alter sympathetic function and drinking, 2 well-known effects of central Ang II, Feng et al, in this issue of Circulation Research,8 used adenoviral transfection techniques to overexpress ACE2 in the mouse . . . [Full Text of this Article]


Related Article:

Angiotensin-Converting Enzyme 2 Overexpression in the Subfornical Organ Prevents the Angiotensin II–Mediated Pressor and Drinking Responses and Is Associated With Angiotensin II Type 1 Receptor Downregulation
Yumei Feng, Xinping Yue, Huijing Xia, Sharell M. Bindom, Peter J. Hickman, Catalin M. Filipeanu, Guangyu Wu, and Eric Lazartigues
Circ. Res. 2008 102: 729-736. [Abstract] [Full Text] [PDF]