Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1987-10-13
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0022-2631
pubmed:author
pubmed:issnType
Print
pubmed:volume
97
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
251-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
Ionic channels and membrane hyperpolarization in human macrophages.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't