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Hypertension. 2008;51:1259-1264
Published online before print March 17, 2008, doi: 10.1161/HYPERTENSIONAHA.108.110924
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(Hypertension. 2008;51:1259.)
© 2008 American Heart Association, Inc.


Brief Reviews

Critical Review of Prorenin and (Pro)renin Receptor Research

Duncan J. Campbell

From the St Vincent’s Institute of Medical Research and Department of Medicine, University of Melbourne, St Vincent’s Hospital, Fitzroy, Victoria, Australia.

Correspondence to Duncan J. Campbell, St Vincent’s Institute of Medical Research, 41 Victoria Parade, Fitzroy, Victoria 3065, Australia. E-mail dcampbell@svi.edu.au


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


*    Introduction
 
The renin-angiotensin system (RAS) plays an important role in cardiovascular and renal physiology and disease, and the benefits of angiotensin-converting enzyme inhibitor, angiotensin type 1 receptor blocker, and renin inhibitor therapies are mediated in part by their modification of the levels and actions of angiotensin peptides. Despite its long history, the RAS remains an active area of research. Contrary to the classical view of the RAS as an endocrine system whereby kidney-secreted renin acts on circulating angiotensinogen to produce angiotensin peptides in the circulation, it is now recognized that tissues are the main sites of angiotensin peptide formation by the action of plasma- (kidney-) derived renin on plasma-derived and locally synthesized angiotensinogen.1–3 A receptor for prorenin and renin was recently identified4,5 that is hereby referred to as the (pro)renin receptor. Prorenin and (pro)renin receptor research offers the exciting possibility of a new paradigm for the RAS whereby renin and prorenin binding to the (pro)renin receptor not only target and facilitate angiotensin generation but also lead to activation of (pro)renin receptor signal transduction pathways distinct from angiotensin II receptor signals.6,7 By revealing novel potential mechanisms of disease pathogenesis, this new paradigm offers the possibility of new therapies that may be more effective than those currently available. It also suggests that stimulation of the (pro)renin receptor by the increased renin and prorenin levels that accompany angiotensin-converting enzyme inhibitor, angiotensin type 1 receptor blocker, and renin inhibitor therapies may attenuate the benefits these therapies.7,8 Recent reviews and editorials have discussed this research.6,9,10 The . . . [Full Text of this Article]




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