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pubmed-article:8957550pubmed:abstractTextIn this paper, we review the hypothesis that activated tissue renin-angiotensin systems play a detrimental role in heart failure. The main arguments for this idea are discussed: a) tissue renin-angiotensin systems behave functionally distinct from the circulating renin-angiotensin system; b) tissue renin-angiotensin systems are activated in heart failure; c) activated tissue renin-angiotensin systems induce cardiovascular dysfunction. Finally, this hypothesis predicts that optimal treatment in heart failure requires the inhibition of tissue renin-angiotensin systems. However, studies pertaining to this prediction are still lacking, particularly in human subjects.lld:pubmed
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pubmed-article:8957550pubmed:authorpubmed-author:LimK AKAlld:pubmed
pubmed-article:8957550pubmed:authorpubmed-author:van GilstW...lld:pubmed
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pubmed-article:8957550pubmed:authorpubmed-author:PintoY MYMlld:pubmed
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pubmed-article:8957550pubmed:volume91 Suppl 2lld:pubmed
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pubmed-article:8957550pubmed:pagination85-90lld:pubmed
pubmed-article:8957550pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:8957550pubmed:year1996lld:pubmed
pubmed-article:8957550pubmed:articleTitleActivated tissue renin-angiotensin systems add to the progression of heart failure.lld:pubmed
pubmed-article:8957550pubmed:affiliationDept. of Cardiology, University of Groningen, The Netherlands.lld:pubmed
pubmed-article:8957550pubmed:publicationTypeJournal Articlelld:pubmed
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