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©2014 Baishideng Publishing Group Inc. All rights reserved.
Renin-angiotensin system in the kidney: What is new?
Fernanda M Ferrão, Jennifer Lowe, Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, Brazil
Fernanda M Ferrão, Lucienne S Lara, Jennifer Lowe, National Institute of Science and Technology for Structural Biology and Bioimaging, Rio de Janeiro 21941-902, Brazil
Lucienne S Lara, Institute of Biomedical Sciences, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, Brazil
Author contributions: Ferrão FM, Lara LS and Lowe J all contributed to this paper, filling all the three conditions established by Baishideng Publishing Group.
Supported by Carlos Chagas Filho Rio de Janeiro State Research Foundation (FAPERJ), National Institute of Science and Technology for Structural Biology and Bioimaging, Brazilian National Research Council (CNPq)
Correspondence to: Jennifer Lowe, MSc, PhD, Laboratório de Físico-Química Biológica, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, UFRJ-CCS-Bloco G-Sala G1-037, Rio de Janeiro 21941-902, Brazil. lowe@biof.ufrj.br
Telephone: +55-21-39386520 Fax: +55-21-22808193
Received: May 26, 2014
Revised: July 7, 2014
Accepted: July 25, 2014
Published online: August 6, 2014
Revised: July 7, 2014
Accepted: July 25, 2014
Published online: August 6, 2014
Core Tip
Core tip: Activation of the angiotensin converting enzyme (ACE)/ Angiotensin II (Ang II)/AT1 axis leads to vasoconstriction, anti-diuresis, anti-natriuresis, release of aldosterone and anti-diuretic hormone, which can result in hypertension, renal and cardiovascular diseases. Inhibition of renin and ACE or blocking AT1 receptor is the most used therapies for heart failure and hypertension. Nevertheless, the discovery of local Ang II synthesis, new Ang II metabolites, receptors and axis of this system, makes possible the development of new drugs and strategies for renal and cardiovascular diseases treatment, such as activation of ACE2/Ang-(1-7)/Mas axis, which presents opposite effects of AT1 activation by Ang II.