Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-1-8
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
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
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0041-008X
pubmed:author
pubmed:issnType
Print
pubmed:volume
152
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
315-26
pubmed:dateRevised
2010-11-18
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
pubmed:year
1998
pubmed:articleTitle
Role of angiotensin II, endothelin-1, and nitric oxide in HgCl2-induced acute renal failure.
pubmed:affiliation
Department of Hygiene and Preventive Medicine, Faculty of Medicine, Saitama Medical School, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't