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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1983-11-23
|
| pubmed:abstractText |
From previous studies, it is known that in the diluting segment, C1- -ions are transported from the tubule lumen into the cell together with Na+ and K+ via a furosemide-sensitive cotransport system. This carrier-mediated process, located in the luminal cell membrane, is driven by the steep "downhill" Na+ gradient (directed from lumen to cell) which is maintained by the ouabain-sensitive Na+/K+-pump at the peritubular cell membrane. C1- -ions are accumulated within the cell cytosol and are supposed to leave the cell by a C1- -conductive pathway. The present experiments, performed in diluting segments of the isolated perfused frog kidney, demonstrate the existence of a significant C1- -permeability of the peritubular cell membrane and its complete inhibition by anthracene-9-COOH. The data indicate that C1- -reabsorption can be reduced not only by the inhibition of luminal C1- -entry (i.e. by furosemide) but also by the blockade of the passive C1- -exit step across the peritubular cell membrane. Since complete inhibition of C1- -permeability reduces transepithelial uphill C1- -transport only to half, the data disclose the existence of an additional C1- -pathway at the peritubular cell membrane.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jul
|
| pubmed:issn |
0031-6768
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
398
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
172-4
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading | |
| pubmed:year |
1983
|
| pubmed:articleTitle |
Anthracene-9-carboxylic acid inhibits renal chloride reabsorption.
|
| pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
|