| The renin-angiotensin system as a primary cause of polyarteritis nodosa in rats. | |
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MedLine Citation:
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PMID: 19432815 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Polyarteritis nodosa is a necrotizing vasculitis of medium-sized arteries of unknown origin. Hypertension is present in 30% of patients with polyarteritis nodosa. In those cases, high renin levels are thought to be secondary to renal involvement. The present study was performed to identify causal factors of polyarteritis nodosa. In cyp1a1ren-2 transgenic rats, vasculitis of medium-sized arteries resembling classical polyarteritis nodosa can be induced. In this model, oral administration of indole-3-carbinol (I3C) activates the liver-specific cyp1a1 promoter, leading to prorenin expression in a dose-dependent manner. After the first 6 weeks of chronic induction with 0.125% I3C, the mean arterial pressure reached a plateau of about 170 mmHg. Ten out of 11 I3C-treated rats, which were chronically instrumented with a telemetric device to measure blood pressure, developed polyarteritis nodosa within 10 weeks of I3C treatment. I3C alone or instrumentation alone did not cause polyarteritis nodosa. The angiotensin-converting enzyme inhibitor captopril completely prevented the development of polyarteritis nodosa, indicating that local angiotensin II generation is a pathogenetic factor in this model. The renin-angiotensin system can play a primary role in the development of polyarteritis nodosa in rats. |
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Authors:
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Barbara S Peters; Beate Kuttler; Andreas Beineke; Gerd Lorenz; Andrea Thiele; Oliver Nicolai; Rainer Rettig; John J Mullins; Jörg Peters |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-05-11 |
Journal Detail:
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Title: Journal of cellular and molecular medicine Volume: 14 ISSN: 1582-4934 ISO Abbreviation: J. Cell. Mol. Med. Publication Date: 2010 Jun |
Date Detail:
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Created Date: 2010-07-23 Completed Date: 2010-10-21 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101083777 Medline TA: J Cell Mol Med Country: England |
Other Details:
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Languages: eng Pagination: 1318-27 Citation Subset: IM |
Affiliation:
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Institute of Physiology, Department of Cardiovascular Medicine, University of Greifswald, Greifswald, Germany. bspeters@gmx.de |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antibodies, Antineutrophil Cytoplasmic / metabolism Antibodies, Antinuclear / metabolism Antigens, CD3 / metabolism Blood Pressure / drug effects Body Weight / drug effects Captopril / pharmacology Cell Movement / drug effects Cytochrome P-450 CYP1A1 / metabolism Indoles / pharmacology Male Polyarteritis Nodosa / enzymology, pathology, physiopathology* Rats Rats, Transgenic Renin / metabolism Renin-Angiotensin System* / drug effects T-Lymphocytes / drug effects Weight Loss / drug effects |
| Grant Support | |
ID/Acronym/Agency:
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//Wellcome Trust |
| Chemical | |
Reg. No./Substance:
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0/Antibodies, Antineutrophil Cytoplasmic; 0/Antibodies, Antinuclear; 0/Antigens, CD3; 0/Indoles; 0/Ren2 protein, rat; 62571-86-2/Captopril; 700-06-1/indole-3-carbinol; EC 1.14.14.1/Cytochrome P-450 CYP1A1; EC 3.4.23.15/Renin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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