This Article Full Text Full Text (PDF) All Versions of this Article: 43/5/943    most recent 01.HYP.0000124669.02394.72v1 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 Carey, R. M. Search for Related Content PubMed PubMed Citation Articles by Carey, R. M.

(Hypertension. 2004;43:943.)
© 2004 American Heart Association, Inc.

Editorial Commentary

Angiotensin Type-1 Receptor Blockade Increases ACE 2 Expression in the Heart

From the Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia Health System, Charlottesville.

Correspondence to Dr Robert M. Carey, P.O. Box 801414, University of Virginia Health System, Charlottesville, VA 22908. E-mail rmc4c@virginia.edu

Key Words: renin II • heart • receptors, angiontensin

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

The renin-angiotensin system (RAS) is a coordinated hormonal cascade, the major effecter of which is angiotensin II (Ang II).^1,2 The RAS regulates blood pressure and fluid and electrolyte balance through actions on the heart, blood vessels, kidneys, and adrenal glands. The classical RAS pathway begins with the biosynthesis, storage, and release of the glycoprotein enzyme renin by the juxtaglomerular cells of the renal afferent arteriole. Renin acts on the circulating precursor angiotensinogen (AGT) to form a dipeptide, angiotensin I (Ang I). Ang I has little or no biological activity but is converted across vascular beds, particularly in the lungs, to the octapeptide Ang II by the action of angiotensin-converting enzyme (ACE), an enzyme with soluble and membrane-bound forms. Most of the ACE is localized on the plasma membranes of vascular endothelial cells and the brush borders of epithelial (eg, renal tubular) cells. A potent vasopressor, Ang II acts at target cells by binding to 1 of 2 G protein-coupled receptors—angiotensin type-1 (AT₁) and type-2 (AT₂) receptors. The vast majority of the cardiovascular, renal, and adrenal actions of Ang II are mediated by the AT₁ receptor, including vascular smooth muscle contraction, aldosterone secretion, dipsogenic responses, adrenergic stimulation, renal sodium reabsorption, and pressor and chronotropic responses. Ang II also binds to AT₂ receptors, inducing a counter-regulatory vasodilatation that is largely mediated by bradykinin (BK) and nitric oxide (NO). In addition to the conversion of Ang I to Ang II, ACE also inactivates two vasodilator peptides, BK and kallidin. Thus, ACE . . . [Full Text of this Article]

This article has been cited by other articles:

				C. M. Ferrario, A. J. Trask, and J. A. Jessup Advances in biochemical and functional roles of angiotensin-converting enzyme 2 and angiotensin-(1-7) in regulation of cardiovascular function Am J Physiol Heart Circ Physiol, December 1, 2005; 289(6): H2281 - H2290. [Abstract] [Full Text] [PDF]

				C. M. Ferrario Myocardial infarction increases ACE2 expression in rat and humans Eur. Heart J., June 1, 2005; 26(11): 1141 - 1141. [Full Text] [PDF]