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Published in: Current Hypertension Reports 1/2013

01-02-2013 | Hypertension and the Kidney (RM Carey and A Mimran, Section Editors)

Update on the Angiotensin AT2 Receptor

Authors: Claudia A. McCarthy, Robert E. Widdop, Kate M. Denton, Emma S. Jones

Published in: Current Hypertension Reports | Issue 1/2013

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Abstract

It is quite well established that activation of the AT2 receptor (AT2R) provides a counter-regulatory role to AT1R overactivity, particularly during pathological conditions. Indeed, a potential therapeutic role for the AT2R is currently being promulgated with the introduction of novel AT2R ligands such as compound 21 (C21). In this brief review, we will focus on recent evidence to suggest that AT2R exhibits promising organ protection in the context of the heart, kidney and brain, with inflammation and gender influencing outcome. However, this field is not without controversy since the ‘flagship’ ligand C21 has also come under scrutiny, although it is safe to say there is much evidence to support a potentially important role of AT2R in a number of cardiovascular diseases. This report updates recent data in this field.
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go back to reference • Horiuchi M, Iwanami J, Mogi M. Regulation of angiotensin II receptors beyond the classical pathway. Clin Sci. 2012;123:193–203. An excellent recent review summarising a number of aspects of nonclassical Ang signaling that are not covered in the current update.PubMedCrossRef • Horiuchi M, Iwanami J, Mogi M. Regulation of angiotensin II receptors beyond the classical pathway. Clin Sci. 2012;123:193–203. An excellent recent review summarising a number of aspects of nonclassical Ang signaling that are not covered in the current update.PubMedCrossRef
Metadata
Title
Update on the Angiotensin AT2 Receptor
Authors
Claudia A. McCarthy
Robert E. Widdop
Kate M. Denton
Emma S. Jones
Publication date
01-02-2013
Publisher
Current Science Inc.
Published in
Current Hypertension Reports / Issue 1/2013
Print ISSN: 1522-6417
Electronic ISSN: 1534-3111
DOI
https://doi.org/10.1007/s11906-012-0321-4

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