|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0010453,
umls-concept:C0025914,
umls-concept:C0026809,
umls-concept:C0026882,
umls-concept:C0027713,
umls-concept:C0205225,
umls-concept:C0205349,
umls-concept:C0456148,
umls-concept:C0521116,
umls-concept:C0596019,
umls-concept:C1413365
|
|
pubmed:issue |
4
|
|
pubmed:dateCreated |
2003-3-6
|
|
pubmed:abstractText |
The role of cystic fibrosis transmembrane conductance regulator (CFTR) in the control of Cl(-) currents was studied in mouse kidney. Whole cell clamp was used to analyze Cl(-) currents in primary cultures of proximal and distal convoluted and cortical collecting tubules from wild-type (WT) and cftr knockout (KO) mice. In WT mice, forskolin activated a linear Cl(-) current only in distal convoluted and cortical collecting tubule cells. This current was not recorded in KO mice. In both mice, Ca(2+)-dependent Cl(-) currents were recorded in all segments. In WT mice, volume-sensitive Cl(-) currents were implicated in regulatory volume decrease during hypotonicity. In KO mice, regulatory volume decrease and swelling-activated Cl(-) current were impaired but were restored by adenosine perfusion. Extracellular ATP also restored swelling-activated Cl(-) currents. The effect of ATP or adenosine was blocked by 8-cyclopentyl-1,3-diproxylxanthine. The ecto-ATPase inhibitor ARL-67156 inhibited the effect of hypotonicity and ATP. Finally, in KO mice, volume-sensitive Cl(-) currents are potentially functional, but the absence of CFTR precludes their activation by extracellular nucleosides. This observation strengthens the hypothesis that CFTR is a modulator of ATP release in epithelia.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Apr
|
|
pubmed:issn |
1931-857X
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
284
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
F796-811
|
|
pubmed:dateRevised |
2011-4-28
|
|
pubmed:meshHeading |
pubmed-meshheading:12475744-Adenosine,
pubmed-meshheading:12475744-Animals,
pubmed-meshheading:12475744-Calcium,
pubmed-meshheading:12475744-Cell Size,
pubmed-meshheading:12475744-Cells, Cultured,
pubmed-meshheading:12475744-Chloride Channels,
pubmed-meshheading:12475744-Chlorides,
pubmed-meshheading:12475744-Cyclic AMP,
pubmed-meshheading:12475744-Cystic Fibrosis Transmembrane Conductance Regulator,
pubmed-meshheading:12475744-Enzyme Inhibitors,
pubmed-meshheading:12475744-Forskolin,
pubmed-meshheading:12475744-Hypotonic Solutions,
pubmed-meshheading:12475744-Kidney Tubules,
pubmed-meshheading:12475744-Mice,
pubmed-meshheading:12475744-Mice, Inbred C57BL,
pubmed-meshheading:12475744-Mice, Inbred CFTR,
pubmed-meshheading:12475744-Mice, Knockout,
pubmed-meshheading:12475744-Mutation,
pubmed-meshheading:12475744-Nephrons,
pubmed-meshheading:12475744-Patch-Clamp Techniques,
pubmed-meshheading:12475744-Transfection
|
|
pubmed:year |
2003
|
|
pubmed:articleTitle |
CFTR null mutation altered cAMP-sensitive and swelling-activated Cl- currents in primary cultures of mouse nephron.
|
|
pubmed:affiliation |
Unité Mixte de Recherche Centre National de la Recherche Scientifique 6548, Université de Nice-Sophia Antipolis, 06108 Nice Cedex 2, France.
|
|
pubmed:publicationType |
Journal Article
|
