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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
|
| pubmed:dateCreated |
1992-8-6
|
| pubmed:abstractText |
We sought to determine whether extracellular Ca2+ (Ca2+e) and K+ (K+e) play essential roles in the normal functioning of cardiac K+ channels. Reports by others have shown that removal of Ca2+e and K+e alters the gating properties of neural delayed rectifier (IK) and A-type K+ currents, resulting in a loss of normal cation selectivity and voltage-dependent gating. We found that removal of Ca2+e and K+e from the solution bathing guinea pig ventricular myocytes often induced a leak conductance, but did not affect the ionic selectivity or time-dependent activation and deactivation properties of IK. The effect of [K+]e on the magnitude of the two components of cardiac IK was also examined. IK in guinea pig myocytes is comprised of two distinct types of currents: IKr (rapidly activating, rectifying) and IKs (slowly activating). The differential effect of Ca2+e on the two components of IK (previously shown to shift the voltage dependence of activation of the two currents in opposite directions) was exploited to determine the role of K+e on the magnitude of IKs and IKr. Lowering [K+]e from 4 to 0 mM increased IKs, as expected from the change in driving force for K+, but decreased IKr. The differential effect of [K+]e on the two components of cardiac IK may explain the reported discrepancies regarding modulation of cardiac IK conductance by this cation.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
0031-6768
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
420
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
180-6
|
| pubmed:dateRevised |
2003-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:1620577-Animals,
pubmed-meshheading:1620577-Calcium,
pubmed-meshheading:1620577-Cells, Cultured,
pubmed-meshheading:1620577-Extracellular Space,
pubmed-meshheading:1620577-Guinea Pigs,
pubmed-meshheading:1620577-Ion Channel Gating,
pubmed-meshheading:1620577-Membrane Potentials,
pubmed-meshheading:1620577-Myocardium,
pubmed-meshheading:1620577-Potassium,
pubmed-meshheading:1620577-Potassium Channels
|
| pubmed:year |
1992
|
| pubmed:articleTitle |
Role of external Ca2+ and K+ in gating of cardiac delayed rectifier K+ currents.
|
| pubmed:affiliation |
Department of Pharmacology, Merck Sharp & Dohme Research Laboratories, West Point, PA 19486.
|
| pubmed:publicationType |
Journal Article
|