Linked Life Data

11889576

Source:http://linkedlifedata.com/resource/pubmed/id/11889576

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5-6
pubmed:dateCreated
2002-3-12
pubmed:abstractText
We studied the effects of hypertonic stress on ion transport and cell volume regulation (regulatory volume increase; RVI) in the human tumor cell-line HepG2. Ion conductances were monitored in intracellular current-clamp measurements with rapid ion-substitutions and in whole-cell patch-clamp recordings; intracellular pH buffering capacity and activation of Na(+)/H(+) antiport were determined fluorometrically; the rates of Na(+)-K(+)-2Cl(-) symport and Na(+)/K(+)-ATPase were quantified on the basis of time-dependent and furosemide- or ouabain-sensitive (86)Rb(+) uptake, respectively; changes in cell volume were recorded by means of confocal laser-scanning microscopy. It was found that hypertonic conditions led to the activation of a cation conductance that was inhibited by Gd(3+), flufenamate as well as amiloride, but not by benzamil or ethyl-isopropyl-amiloride (EIPA). Most likely, this cation conductance was non-selective for Na(+) over K(+). Hypertonic stress did not change K(+) conductance, whereas possible changes in Cl(-) conductance remain ambiguous. The contribution of Na(+)/H(+)antiport to the RVI process appeared to be minor. Under hypertonic conditions an approximately 3.5-fold stimulation of Na(+)-K(+)-2Cl(-)symport was observed but this transporter did not significantly contribute to the overall RVI process. Hypertonic stress did not increase the activity of Na(+)/K(+)-ATPase, which even under isotonic conditions appeared to be working at its limit. It is concluded that the main mechanism in the RVI of HepG2 cells is the activation of a novel non-selective cation conductance. In contrast, there is little if any contribution of K(+) conductance, Na(+)/H(+) antiport, Na(+)-K(+)-2Cl(-) symport, and Na(+)/K(+)-ATPase to this process.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
443
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
779-90
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11889576-Alkalies, pubmed-meshheading:11889576-Amiloride, pubmed-meshheading:11889576-Carcinoma, Hepatocellular, pubmed-meshheading:11889576-Diuretics, pubmed-meshheading:11889576-Hepatocytes, pubmed-meshheading:11889576-Humans, pubmed-meshheading:11889576-Hydrogen-Ion Concentration, pubmed-meshheading:11889576-Hypertonic Solutions, pubmed-meshheading:11889576-Liver Neoplasms, pubmed-meshheading:11889576-Osmotic Pressure, pubmed-meshheading:11889576-Patch-Clamp Techniques, pubmed-meshheading:11889576-Potassium, pubmed-meshheading:11889576-Sodium, pubmed-meshheading:11889576-Sodium-Hydrogen Antiporter, pubmed-meshheading:11889576-Sodium-Potassium-Chloride Symporters, pubmed-meshheading:11889576-Sodium-Potassium-Exchanging ATPase, pubmed-meshheading:11889576-Tumor Cells, Cultured, pubmed-meshheading:11889576-Water-Electrolyte Balance
pubmed:year
2002
pubmed:articleTitle
Ionic mechanisms of regulatory volume increase (RVI) in the human hepatoma cell-line HepG2.
pubmed:affiliation
Max-Planck-Institut für molekulare Physiologie, Abteilung Epithelphysiologie, Postfach 500247, 44202 Dortmund, Germany, frank.wehner@mpi-dortmund.mpg.de
pubmed:publicationType
Journal Article