This Article Full Text Full Text (PDF) All Versions of this Article: 46/5/1097    most recent 01.HYP.0000185149.56516.0av1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Brosnihan, K. B. Articles by Chappell, M. C. Search for Related Content PubMed PubMed Citation Articles by Brosnihan, K. B. Articles by Chappell, M. C. Related Collections Other hypertension Related Article

(Hypertension. 2005;46:1097.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Does the Angiotensin-Converting Enzyme (ACE)/ACE2 Balance Contribute to the Fate of Angiotensin Peptides in Programmed Hypertension?

K. Bridget Brosnihan; Liomar A.A. Neves; Mark C. Chappell

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

Correspondence to K. Bridget Brosnihan, Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Medical Center Blvd, Winston-Salem, NC. E-mail bbrosnih@wfubmc.edu

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 key role in blood pressure regulation, fluid and electrolyte balance, cellular growth, thirst, and cardiac/renal function. The classic system primarily involves 2 enzymes: renin, which cleaves angiotensinogen to the inactive decapeptide angiotensin (Ang) I; and Ang-converting enzyme (ACE), a dipeptidyl carboxypeptidase that hydrolyzes Ang I to the octapeptide Ang II. The elucidation of the ACE pathway in parallel with potent and selective ACE inhibitors is clearly a pivotal achievement in our understanding of the RAS and in attaining effective therapies for hypertension and end organ damage. Indeed, ACE inhibitors attenuate Ang II formation and augment the levels of the heptapeptide Ang (1–7), a peptide that counterbalances the actions of Ang II on blood pressure and cellular growth through a unique receptor system. Ang II mediates the majority of its actions at the Ang II type 1 (AT₁) receptor, including the stimulation of vasoconstriction, sodium retention, cellular growth, and oxidative stress, whereas recent studies show that Ang (1–7) at the AT_1–7 or mas receptor and Ang II via the AT₂ receptor subtype counterregulate the actions of Ang II at the AT₁ receptor.

The discovery of the ACE homolog ACE2 provides further evidence that the RAS is far more complex than originally thought. The enzymatic cascade of the RAS should now encompass the ACE2-dependent pathways that directly yield Ang (1–9) from Ang I and degrade Ang II to Ang (1–7) (Figure). The interplay between ACE and ACE2 that may govern the formation and . . . [Full Text of this Article]

Related Article:

Angiotensin-Converting Enzyme 2 (ACE2) and ACE Activities Display Tissue-Specific Sensitivity to Undernutrition-Programmed Hypertension in the Adult Rat

Guillaume Rivière, Annie Michaud, Christophe Breton, Gilles VanCamp, Christine Laborie, Mihaela Enache, Jean Lesage, Sylvie Deloof, Pierre Corvol, and Didier Vieau
Hypertension 2005 46: 1169-1174. [Abstract] [Full Text] [PDF]

This article has been cited by other articles:

				R. Zhang, Y. Wu, M. Zhao, C. Liu, L. Zhou, S. Shen, S. Liao, K. Yang, Q. Li, and H. Wan Role of HIF-1{alpha} in the regulation ACE and ACE2 expression in hypoxic human pulmonary artery smooth muscle cells Am J Physiol Lung Cell Mol Physiol, October 1, 2009; 297(4): L631 - L640. [Abstract] [Full Text] [PDF]

				H. A. Shaltout, J. P. Figueroa, J. C. Rose, D. I. Diz, and M. C. Chappell Alterations in Circulatory and Renal Angiotensin-Converting Enzyme and Angiotensin-Converting Enzyme 2 in Fetal Programmed Hypertension Hypertension, February 1, 2009; 53(2): 404 - 408. [Abstract] [Full Text] [PDF]

				V. Koka, X. R. Huang, A. C.K. Chung, W. Wang, L. D. Truong, and H. Y. Lan Angiotensin II Up-Regulates Angiotensin I-Converting Enzyme (ACE), but Down-Regulates ACE2 via the AT1-ERK/p38 MAP Kinase Pathway Am. J. Pathol., May 1, 2008; 172(5): 1174 - 1183. [Abstract] [Full Text] [PDF]

				N. B. Ojeda, D. Grigore, E. B. Robertson, and B. T. Alexander Estrogen Protects Against Increased Blood Pressure in Postpubertal Female Growth Restricted Offspring Hypertension, October 1, 2007; 50(4): 679 - 685. [Abstract] [Full Text] [PDF]