| pubmed-article:9174990 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9174990 | lifeskim:mentions | umls-concept:C0015859 | lld:lifeskim |
| pubmed-article:9174990 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:9174990 | lifeskim:mentions | umls-concept:C2339371 | lld:lifeskim |
| pubmed-article:9174990 | lifeskim:mentions | umls-concept:C0248868 | lld:lifeskim |
| pubmed-article:9174990 | lifeskim:mentions | umls-concept:C0006776 | lld:lifeskim |
| pubmed-article:9174990 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:9174990 | lifeskim:mentions | umls-concept:C1948027 | lld:lifeskim |
| pubmed-article:9174990 | pubmed:dateCreated | 1997-8-8 | lld:pubmed |
| pubmed-article:9174990 | pubmed:abstractText | 1. The effect of Ca(2+)-calmodulin-dependent protein kinase II (CaMKII) on excitation-contraction coupling (E-C coupling) was studied in intact ferret cardiac myocytes using the selective inhibitor KN-93, KN-93 decreased steady-state (SS) twitch [Ca2+]i (by 51%), resting Ca2+ spark frequency (by 88%) and SS sarcoplasmic reticulum (SR) Ca2+ content evaluated by eaffeine application (by 37.5%). 2. Increasing extracellular Ca2+ concentration ([Ca2+]o) to 5 mM in KN-93 restored SR Ca2+ load and Ca2+ spark frequency towards that in control (2 mM Ca2+o), but SS twitch [Ca2+]i was still significantly depressed by KN-93. 3. KN-93 decreased Ca2+ transient amplitude of SS twitches much more strongly than the amplitude of post-rest (PR) twitches. In the control, the time constant (Tau) of [Ca2+]i decline of SS twitches was faster than that for PR twitches. This stimulation-dependent acceleration of [Ca2+]i decline was abolished by KN-93. 4. Voltage-clamp experiments demonstrated that KN-93 significantly inhibited sarcolemmal L-type Ca2+ current (ICa) during repetitive pulses by slowing recovery from inactivation. This may explain the preferential action of KN-93 to suppress SS vs. PR twitches. 5. In KN-93, even when both ICa and SR Ca2+ load were matched to the control levels by manipulation of conditioning voltage-clamp pulses, contraction and twitch Ca2+ transients were still both significantly depressed (to 39 and 49% of control, respectively). 6. Since KN-93 reduced SR Ca2+ release channel (RyR) activity during E-C coupling, even for matched SR Ca2+ load and trigger ICa, we infer that endogenous CaMKII is an important modulator of E-C coupling in intact cardiac myocytes. Effects of KN-93 on ICa and SS twitch [Ca2+]i decline also indicate that endogenous CaMKII may have stimulatory effects on ICa and SR Ca2+ uptake. | lld:pubmed |
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| pubmed-article:9174990 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9174990 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9174990 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9174990 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9174990 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9174990 | pubmed:month | May | lld:pubmed |
| pubmed-article:9174990 | pubmed:issn | 0022-3751 | lld:pubmed |
| pubmed-article:9174990 | pubmed:author | pubmed-author:SatohHH | lld:pubmed |
| pubmed-article:9174990 | pubmed:author | pubmed-author:LORR | lld:pubmed |
| pubmed-article:9174990 | pubmed:author | pubmed-author:BersD MDM | lld:pubmed |
| pubmed-article:9174990 | pubmed:author | pubmed-author:GinsburgK SKS | lld:pubmed |
| pubmed-article:9174990 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9174990 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:9174990 | pubmed:volume | 501 ( Pt 1) | lld:pubmed |
| pubmed-article:9174990 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9174990 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9174990 | pubmed:pagination | 17-31 | lld:pubmed |
| pubmed-article:9174990 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:9174990 | pubmed:meshHeading | pubmed-meshheading:9174990-... | lld:pubmed |
| pubmed-article:9174990 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9174990 | pubmed:articleTitle | The effect of Ca(2+)-calmodulin-dependent protein kinase II on cardiac excitation-contraction coupling in ferret ventricular myocytes. | lld:pubmed |
| pubmed-article:9174990 | pubmed:affiliation | Department of Physiology, Loyola University Chicago, Stritch School of Medicine, Maywood, IL 60153, USA. | lld:pubmed |
| pubmed-article:9174990 | pubmed:publicationType | Journal Article | lld:pubmed |
