| pubmed-article:7517630 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7517630 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:7517630 | lifeskim:mentions | umls-concept:C0034493 | lld:lifeskim |
| pubmed-article:7517630 | lifeskim:mentions | umls-concept:C0596981 | lld:lifeskim |
| pubmed-article:7517630 | lifeskim:mentions | umls-concept:C1522318 | lld:lifeskim |
| pubmed-article:7517630 | lifeskim:mentions | umls-concept:C0205463 | lld:lifeskim |
| pubmed-article:7517630 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:7517630 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:7517630 | pubmed:issue | 6 Pt 1 | lld:pubmed |
| pubmed-article:7517630 | pubmed:dateCreated | 1994-7-29 | lld:pubmed |
| pubmed-article:7517630 | pubmed:abstractText | The properties and function of Ca(2+)-activated K+ (KCa) and voltage-dependent K+ (IK) currents of rabbit coronary myocytes were studied under whole cell voltage-clamp conditions (22 degrees C). Inhibition of KCa by tetraethylammonium chloride (1-10 mM) or charybdotoxin (50-100 nM) suppressed noisy outward rectifying current elicited by 5-s voltage steps or ramp at potentials > 0 mV, reduced the hump of the biphasic ramp current-voltage relation, and shifted by less than +5 mV the potential at which no net steady-state current is recorded (Enet; index of resting membrane potential). Inhibition of steady-state inward Ca2+ currents [ICa(L)] by nifedipine (1 microM) displaced Enet by -11 mV. Analysis of steady-state voltage dependence of IK supported the existence of a "window" current between -50 and 0 mV. 4-Aminopyridine (2 mM) blocked a noninactivating component of IK evoked between -30 and -40 mV, abolished the hump current during ramps, and shifted Enet by more than +15 mV; hump current persisted during 2-min ramp depolarizations and peaked near the maximum overlap of the steady-state activation and inactivation curves of IK (about -22 mV). A threefold rise in extracellular Ca2+ concentration (1.8-5.4 mM) enhanced time-dependent outward K+ current (6.7-fold at +40 mV) and shifted Enet by -30 mV. It is concluded that, under steady-state conditions, IK and ICa(L) play a major role in regulating resting membrane potential at a physiological level of intracellular Ca2+ concentration, with a minor contribution from KCa. However, elevation of intracellular Ca2+ concentration enhances KCa and hyperpolarizes the myocyte to limit Ca2+ entry through ICa(L). | lld:pubmed |
| pubmed-article:7517630 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7517630 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7517630 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7517630 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7517630 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:7517630 | pubmed:issn | 0002-9513 | lld:pubmed |
| pubmed-article:7517630 | pubmed:author | pubmed-author:WaySS | lld:pubmed |
| pubmed-article:7517630 | pubmed:author | pubmed-author:LeungP MPM | lld:pubmed |
| pubmed-article:7517630 | pubmed:author | pubmed-author:LeblancNN | lld:pubmed |
| pubmed-article:7517630 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7517630 | pubmed:volume | 266 | lld:pubmed |
| pubmed-article:7517630 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7517630 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7517630 | pubmed:pagination | C1523-37 | lld:pubmed |
| pubmed-article:7517630 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:7517630 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7517630 | pubmed:articleTitle | Physiological role of Ca(2+)-activated and voltage-dependent K+ currents in rabbit coronary myocytes. | lld:pubmed |
| pubmed-article:7517630 | pubmed:affiliation | Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba, Canada. | lld:pubmed |
| pubmed-article:7517630 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7517630 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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