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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1999-1-8
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pubmed:abstractText |
To elucidate the mechanisms underlying the development of HgCl2-induced acute renal failure (ARF), we examined the expression of endothelin (ET)-1, endothelial (e) nitric oxide synthase (NOS) and inducible (i) NOS, and a role of angiotensin II (ANG II) and tumor necrosis factor (TNF) in glomeruli and cortices from rats at 20 h after exposure of HgCl2. Prepro-ET-1 and iNOS mRNA were significantly increased in glomeruli and cortices from rats with HgCl2-induced ARF. However, eNOS mRNA was markedly decreased in glomeruli of rats with HgCl2-induced ARF. Blockade of the action of endogenous ANG II with TCV-116, an ANG II receptor type 1 antagonist, or prior administration of TNF antibody (Ab) neutralizing TNF bioactivity or aminoguanidine, an iNOS inhibitor, substantially suppressed the increase in the expression of prepro-ET-1 or iNOS mRNA seen in rats with HgCl2-induced ARF. Both TCV-116 and TNF Ab had no effects on the expression of eNOS mRNA. The abundance of ET-1, iNOS, and eNOS proteins was paralleled by the magnitude of each mRNA expression. Additionally, the aggravation of blood urea nitrogen and serum Cr observed in rats with HgCl2-induced ARF were significantly ameliorated together with the alleviation of proximal tubule epithelial cell injury when the expression of prepro-ET-1 or iNOS mRNA was blunted by prior administration of TCV-116 or prior injection of TNF Ab or aminoguanidine. These observations indicate that ANG II, ET-1, and NO may play an important role in the progression of HgCl2-induced ARF through the acceleration of proximal tubule epithelial cell injury and the deterioration of glomerular hemodynamics. In HgCl2-induced ARF, the gene expression of ET-1 or iNOS is at least in part up-regulated at the transcription level by endogenous ANG II or TNF.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Chromium,
http://linkedlifedata.com/resource/pubmed/chemical/Creatinine,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Mercuric Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Nos2 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Peptidyl-Dipeptidase A,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0041-008X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
152
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
315-26
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:9853001-Acute Kidney Injury,
pubmed-meshheading:9853001-Angiotensin II,
pubmed-meshheading:9853001-Animals,
pubmed-meshheading:9853001-Blood Urea Nitrogen,
pubmed-meshheading:9853001-Chromium,
pubmed-meshheading:9853001-Creatinine,
pubmed-meshheading:9853001-Disease Progression,
pubmed-meshheading:9853001-Endothelin-1,
pubmed-meshheading:9853001-Female,
pubmed-meshheading:9853001-Immunohistochemistry,
pubmed-meshheading:9853001-Kidney Tubules,
pubmed-meshheading:9853001-Mercuric Chloride,
pubmed-meshheading:9853001-Nitric Oxide,
pubmed-meshheading:9853001-Nitric Oxide Synthase,
pubmed-meshheading:9853001-Nitric Oxide Synthase Type II,
pubmed-meshheading:9853001-Peptidyl-Dipeptidase A,
pubmed-meshheading:9853001-RNA, Messenger,
pubmed-meshheading:9853001-Rats,
pubmed-meshheading:9853001-Rats, Sprague-Dawley,
pubmed-meshheading:9853001-Renin-Angiotensin System,
pubmed-meshheading:9853001-Tumor Necrosis Factor-alpha
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pubmed:year |
1998
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pubmed:articleTitle |
Role of angiotensin II, endothelin-1, and nitric oxide in HgCl2-induced acute renal failure.
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pubmed:affiliation |
Department of Hygiene and Preventive Medicine, Faculty of Medicine, Saitama Medical School, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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