Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-2-25
pubmed:abstractText
The effect of intracellular protons (Hi+) on the inward rectifier K+ channel of the guinea-pig ventricular cell membrane was examined, using the patch-clamp technique. The inward single-channel current was recorded in "inside-out" and "outside-out" patch configurations, while the pH of the solution perfusing the intra- and extracellular side, respectively, was varied. Low intracellular pH (pHi), but not low extracellular pH, inhibited the channel. Low pHi reduced the unit amplitude, which was about 20% smaller at pHi 6.0 than that at pHi 7.4 at every voltage tested. The slope conductance decreased from 41.7 pS at pHi 7.4 to 35.1 pS at pHi 6.0. Low pHi also reduced the channel activity without apparent voltage dependence. The concentration/response curve indicated the half-maximum inhibition at pHi 6.11 and a Hill coefficient of 2.52. Lowering the pHi from 7.4 to 6.0 did not affect the distributions of the open times and the closed times below 50 ms, while the time constant of the histogram constructed from closings longer than 50 ms was approximately doubled. These results indicate that the inward rectifier K+ channel in ventricular myocytes is inhibited by H+ from the intracellular side. This might contribute to the depolarization of the resting membrane potential induced by intracellular acidosis during myocardial ischaemia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
422
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
280-6
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Intracellular protons inhibit inward rectifier K+ channel of guinea-pig ventricular cell membrane.
pubmed:affiliation
Laboratorium voor Fysiologie, Katholieke Universiteit Leuven, Belgium.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't