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NDT Advance Access originally published online on January 27, 2007
Nephrology Dialysis Transplantation 2007 22(5):1288-1292; doi:10.1093/ndt/gfl846
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Prorenin and the (pro)renin receptor—an update

A. H. Jan Danser, Wendy W. Batenburg and Joep H. M. van Esch

Department of Pharmacology, Erasmus MC, Dr Molewaterplein 50, 3015 GE Rotterdam, The Netherlands

Correspondence and offprint requests to: Prof. Dr A. H. J. Danser, PhD, Department of Pharmacology, Room EE1418b, Erasmus MC, Dr Molewaterplein 50, 3015 GE Rotterdam, The Netherlands. Email: a.danser@erasmusmc.nl

Keywords: angiotensin; diabetes; fibrosis; heart; hypertrophy; kidney; MAP kinase; prorenin; (pro)renin receptor; renin

The first 150 words of the full text of this article appear below.



   Introduction
 
Blockers of the renin–angiotensin system (RAS) are widely used for the treatment of cardiovascular and renal diseases. It is generally assumed that the beneficial effects of these drugs are due, at least in part, to blockade of the generation or action of angiotensin (Ang) II at tissue sites [1]. According to this concept, Ang II is generated at tissue sites rather than in circulating blood. Multiple lines of evidence support this idea [2–5]. Remarkably, however, although several RAS components are locally expressed [e.g. ACE, Ang II type 1 (AT1) and type 2 (AT2) receptors] [6–8], thereby allowing such local activity, renin is not [9,10]. Thus, the renin required for local Ang production is sequestered from the circulation, i.e. is kidney-derived. Importantly, renin has an inactive precursor, prorenin. Prorenin is released constitutively from the kidney, and its blood plasma . . . [Full Text of this Article]



   What does prorenin do?
 


   The (pro)renin receptor
 


   Angiotensin-independent effects of prorenin
 


   Summary and future prospects
 

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