| Increased expression of the renin-angiotensin system and mast cell density but not of angiotensin-converting enzyme II in late stages of human heart failure. | |
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MedLine Citation:
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PMID: 16962475 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: The activation of the renin-angiotensin system (RAS) contributes to the progression of left ventricular dysfunction. A novel human homologue of the angiotensin-converting enzyme (ACE), named ACE2, has been described but its role in human heart failure (HF) has not been elucidated. Besides, there is controversy as to whether the major angiotensin II-forming-activity in heart is ACE or chymase released from mast cells. Furthermore, long-term blockade of nitric oxide (NO) synthesis has been shown to increase ACE activity. To assess the locally activated vasoactive mediators that may contribute to the ventricular deterioration process, we sought to simultaneously analyze their expression in failing hearts. METHODS: We analyzed left ventricular biopsies from 30 patients with heart failure undergoing heart transplantation and 12 organ donors. The mRNA levels of ACE, ACE2, chymase and endothelial nitric oxide synthase (eNOS), were quantified by real-time polymerase chain reaction and mast cell density was assessed by immunohistochemistry. The mRNA levels of the atrial natriuretic peptide (ANP) and the brain natriuretic peptide (BNP) were also quantified as controls. RESULTS: There was higher ACE and chymase mRNA expression and mast cell density in failing than in control myocardium and no changes in ACE2 expression were detected. eNOS mRNA levels were lower in failing hearts. Both ANP and BNP expression were higher in pathological than in control samples. CONCLUSIONS: These data document a decompensation of vasoactive systems that may contribute to the progressive impairment of the myocardial function in HF. On the other hand, ACE2 mRNA expression is not altered in human end-stage HF. |
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Authors:
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Montserrat Batlle; Eulàlia Roig; Fèlix Perez-Villa; Sergio Lario; Pilar Cejudo-Martin; Ester García-Pras; José Ortiz; Mercé Roqué; Josefina Orús; Montserrat Rigol; Magdalena Heras; José Ramírez; Wladimiro Jimenez |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2006-08-09 |
Journal Detail:
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Title: The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation Volume: 25 ISSN: 1557-3117 ISO Abbreviation: J. Heart Lung Transplant. Publication Date: 2006 Sep |
Date Detail:
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Created Date: 2006-09-11 Completed Date: 2006-10-24 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9102703 Medline TA: J Heart Lung Transplant Country: United States |
Other Details:
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Languages: eng Pagination: 1117-25 Citation Subset: IM |
Affiliation:
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Experimental Cardiology Laboratory, Hospital Clínic de Barcelona and Institut d'Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain. mbatlle@clinic.ub.es |
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Aged Atrial Natriuretic Factor / genetics, metabolism Biopsy Cardiac Output, Low / genetics, metabolism*, pathology* Cell Count Chymases Disease Progression Female Gene Expression Regulation Gene Expression Regulation, Enzymologic Humans Male Mast Cells / metabolism, pathology* Middle Aged Natriuretic Peptide, Brain / genetics, metabolism Nitric Oxide Synthase Type III / genetics, metabolism Peptidyl-Dipeptidase A / genetics*, metabolism RNA, Messenger / genetics, metabolism Renin-Angiotensin System / genetics, physiology* Serine Endopeptidases / genetics, metabolism Ventricular Dysfunction, Left / genetics, metabolism, pathology |
| Chemical | |
Reg. No./Substance:
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0/RNA, Messenger; 114471-18-0/Natriuretic Peptide, Brain; 85637-73-6/Atrial Natriuretic Factor; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 3.4.15.1/Peptidyl-Dipeptidase A; EC 3.4.17.-/angiotensin converting enzyme 2; EC 3.4.21.-/Serine Endopeptidases; EC 3.4.21.39/Chymases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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