Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1991-3-11
pubmed:abstractText
1. The p-aminophenol (pAP) model of tubular necrosis displays elevated tubular pressures equivalent to 'stop-flow', with low glomerular filtration rate (GFR) but maintained blood flow and urine output. Renal function, micropuncture, and morphological studies were performed in anaesthetized rats to examine the causes of filtration failure. 2. At the height of pAP-induced renal failure proximal tubular fluid reabsorption (Jv(a] was markedly reduced while proximal and distal free-flow rates measured by tubular fluid collections during venting of the nephron were not significantly different from saline-injected controls. Renal blood flow was maintained over the 4 h observation period despite extensive and selective proximal tubular necrosis. There was no temporal relationship between increased tubular pressure and cast formation. 3. Maintained blood and tubular fluid flow rates indicate that activation of tubuloglomerular feedback plays little or no part in pAP-induced renal failure, which is apparently due to high fluid flow resistance in the region of the connecting tubule, late distal convolution or collecting ducts. Morphological appearances were consistent with compression of these segments.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0305-1870
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
613-26
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Filtration failure induced by p-aminophenol in rats is due to raised intratubular pressure and not changes in glomerular function.
pubmed:affiliation
Department of Physiology University of Melbourne, Parkville, Victoria Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't