Linked Life Data

1324512

Source:http://linkedlifedata.com/resource/pubmed/id/1324512

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1992-9-22
pubmed:abstractText
Although some humoral and neural factors have been implicated in the persistent vasoconstriction characterizing many forms of acute renal failure, the mechanisms for this abnormal vascular function have remained largely unresolved. Several factors previously postulated to have a role in acute renal failure have been shown to enhance endothelin (Et) production or gene expression. We studied the potential pathophysiologic role for Et in several models of acute renal failure, including postischemia, endotoxin, and cyclosporine (Cy) nephrotoxicity. We have found that, in vivo, Cy (and also endotoxin) elevates circulating Et. We further showed that antagonizing Et's action with Et antibody ameliorates renal vasoconstriction following renal ischemia, Cy, and endotoxin administration. Additionally, our studies showed that even after circulating levels of Et decrease (following Cy), there is upregulation in Et receptors in the kidneys. Overall, endothelin appears to feature prominently in the pathophysiologic processes occurring during several forms of acute renal failure.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0886-022X
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
345-50
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Endothelin and cyclosporine nephrotoxicity.
pubmed:affiliation
Pediatric Nephrology, Vanderbilt University School of Medicine.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't