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New roles for renin and prorenin in heart failure and cardiorenal crosstalk

The renin-angiotensin-aldosterone-system (RAAS) plays a central role in the pathophysiology of heart failure and cardiorenal interaction. Drugs interfering in the RAAS form the pillars in treatment of heart failure and cardiorenal syndrome. Although RAAS inhibitors improve prognosis, heart failure–a...

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Autores principales: Schroten, Nicolas F., Gaillard, Carlo A. J. M., van Veldhuisen, Dirk J., Szymanski, Mariusz K., Hillege, Hans L., de Boer, Rudolf A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer US 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310995/
https://www.ncbi.nlm.nih.gov/pubmed/21695549
http://dx.doi.org/10.1007/s10741-011-9262-2
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author Schroten, Nicolas F.
Gaillard, Carlo A. J. M.
van Veldhuisen, Dirk J.
Szymanski, Mariusz K.
Hillege, Hans L.
de Boer, Rudolf A.
author_facet Schroten, Nicolas F.
Gaillard, Carlo A. J. M.
van Veldhuisen, Dirk J.
Szymanski, Mariusz K.
Hillege, Hans L.
de Boer, Rudolf A.
author_sort Schroten, Nicolas F.
collection PubMed
description The renin-angiotensin-aldosterone-system (RAAS) plays a central role in the pathophysiology of heart failure and cardiorenal interaction. Drugs interfering in the RAAS form the pillars in treatment of heart failure and cardiorenal syndrome. Although RAAS inhibitors improve prognosis, heart failure–associated morbidity and mortality remain high, especially in the presence of kidney disease. The effect of RAAS blockade may be limited due to the loss of an inhibitory feedback of angiotensin II on renin production. The subsequent increase in prorenin and renin may activate several alternative pathways. These include the recently discovered (pro-) renin receptor, angiotensin II escape via chymase and cathepsin, and the formation of various angiotensin subforms upstream from the blockade, including angiotensin 1–7, angiotensin III, and angiotensin IV. Recently, the direct renin inhibitor aliskiren has been proven effective in reducing plasma renin activity (PRA) and appears to provide additional (tissue) RAAS blockade on top of angiotensin-converting enzyme and angiotensin receptor blockers, underscoring the important role of renin, even (or more so) under adequate RAAS blockade. Reducing PRA however occurs at the expense of an increase plasma renin concentration (PRC). PRC may exert direct effects independent of PRA through the recently discovered (pro-) renin receptor. Additional novel possibilities to interfere in the RAAS, for instance using vitamin D receptor activation, as well as the increased knowledge on alternative pathways, have revived the question on how ideal RAAS-guided therapy should be implemented. Renin and prorenin are pivotal since these are at the base of all of these pathways.
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spelling pubmed-33109952012-03-27 New roles for renin and prorenin in heart failure and cardiorenal crosstalk Schroten, Nicolas F. Gaillard, Carlo A. J. M. van Veldhuisen, Dirk J. Szymanski, Mariusz K. Hillege, Hans L. de Boer, Rudolf A. Heart Fail Rev Article The renin-angiotensin-aldosterone-system (RAAS) plays a central role in the pathophysiology of heart failure and cardiorenal interaction. Drugs interfering in the RAAS form the pillars in treatment of heart failure and cardiorenal syndrome. Although RAAS inhibitors improve prognosis, heart failure–associated morbidity and mortality remain high, especially in the presence of kidney disease. The effect of RAAS blockade may be limited due to the loss of an inhibitory feedback of angiotensin II on renin production. The subsequent increase in prorenin and renin may activate several alternative pathways. These include the recently discovered (pro-) renin receptor, angiotensin II escape via chymase and cathepsin, and the formation of various angiotensin subforms upstream from the blockade, including angiotensin 1–7, angiotensin III, and angiotensin IV. Recently, the direct renin inhibitor aliskiren has been proven effective in reducing plasma renin activity (PRA) and appears to provide additional (tissue) RAAS blockade on top of angiotensin-converting enzyme and angiotensin receptor blockers, underscoring the important role of renin, even (or more so) under adequate RAAS blockade. Reducing PRA however occurs at the expense of an increase plasma renin concentration (PRC). PRC may exert direct effects independent of PRA through the recently discovered (pro-) renin receptor. Additional novel possibilities to interfere in the RAAS, for instance using vitamin D receptor activation, as well as the increased knowledge on alternative pathways, have revived the question on how ideal RAAS-guided therapy should be implemented. Renin and prorenin are pivotal since these are at the base of all of these pathways. Springer US 2011-06-22 2012 /pmc/articles/PMC3310995/ /pubmed/21695549 http://dx.doi.org/10.1007/s10741-011-9262-2 Text en © The Author(s) 2011 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Article
Schroten, Nicolas F.
Gaillard, Carlo A. J. M.
van Veldhuisen, Dirk J.
Szymanski, Mariusz K.
Hillege, Hans L.
de Boer, Rudolf A.
New roles for renin and prorenin in heart failure and cardiorenal crosstalk
title New roles for renin and prorenin in heart failure and cardiorenal crosstalk
title_full New roles for renin and prorenin in heart failure and cardiorenal crosstalk
title_fullStr New roles for renin and prorenin in heart failure and cardiorenal crosstalk
title_full_unstemmed New roles for renin and prorenin in heart failure and cardiorenal crosstalk
title_short New roles for renin and prorenin in heart failure and cardiorenal crosstalk
title_sort new roles for renin and prorenin in heart failure and cardiorenal crosstalk
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310995/
https://www.ncbi.nlm.nih.gov/pubmed/21695549
http://dx.doi.org/10.1007/s10741-011-9262-2
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