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NDT Advance Access originally published online on April 22, 2008
Nephrology Dialysis Transplantation 2008 23(8):2474-2476; doi:10.1093/ndt/gfn184
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Renin inhibition and atherosclerosis*

Friedrich C. Luft

Medical Faculty of the Charité, Helios Klinikum-Berlin, Experimental and Clinical Research Center, Max Delbrück Center for Molecular Medicine, Berlin, Germany

Correspondence and offprint requests to: Friedrich Luft, Experimental and Clinical Research Center, Robert-Rössle Strasse 10, 13125 Berlin, Germany. Tel: +49-30-9406-4249; Fax: +49-30-9406-4220; E-mail: luft@charite.de, fluft@berlin.helios-kliniken.de

Keywords: ACE inhibitors; aliskiren; angiotensin II; bone marrow; renin

The first 10% of the full text of this article appears below.

Angiotensin II (Ang II) has long been considered the major bioactive effector molecule of the renin–angiotensin system and is recognized as a major contributor to hypercholesterolaemia-induced atherosclerosis [1,2]. LDL-receptor-deficient and apoE-deficient mice have been intensively investigated in this regard. Chronic Ang II infusions in such mice accelerate atherosclerosis and promote aneurysm formation [3]. Angiotensin converting enzyme (ACE) inhibitors and angiotensin AT1 receptor blockers (ARB) reduce the atherosclerotic lesion size [3]. The results would suggest that reduced Ang II levels and decreased signalling through AT1 receptors are responsible for the salubrious effects of these drugs. However, some have argued that perhaps increased signalling via AT2 receptors in the case of ARB or perhaps the bioactive angiotensin peptides Ang III, Ang IV or Ang (1–7) play a role. The latter molecule is said to exert protective effects by . . . [Full Text of this Article]



   Clinical perspective
 

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