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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1987-10-13
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pubmed:abstractText |
Microelectrode impalement of human macrophages evokes a transient hyperpolarizing response (HR) of the membrane potential. This HR was found to be dependent on the extracellular concentration of K+ but not on that of Na+ or Cl-. It was not influenced by low temperature (12 degrees C) or by 0.2 mM ouabain, but was blocked by 0.2 mM quinine or 0.2 mM Mg2+-EGTA. These findings indicate that the HR in human macrophages is caused by the activation of a K+ (Ca2+) conductance. Two types of ionic channels were identified in intact cells by use of the patch-clamp technique in the cell-attached-patch configuration, low and high-conductance voltage-dependent K+ channels. The low-conductance channels had a mean conductance of 38 pS with Na+-saline and 32 pS with K+-saline in the pipette. The high-conductance channels had a conductance of 101 and 114 pS with Na+- and K+-saline in the pipette, respectively. Cell-attached patch measurements made during evocation of an HR by microelectrode penetration showed enhanced channel activity associated with the development of the HR. These channels were also high-conductance channels (171 pS with Na+- and 165 pS K+-saline in the pipette) and were voltage dependent. They were, however, active at less positive potentials than the high-conductance K+ channels seen prior to the microelectrode-evoked HR. It is concluded that the high-conductance voltage-dependent ionic channels active during the HR in human macrophages contribute to the development of the HR.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0022-2631
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
97
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
251-8
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading | |
pubmed:year |
1987
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pubmed:articleTitle |
Ionic channels and membrane hyperpolarization in human macrophages.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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