pubmed-article:3162323 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:3162323 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:3162323 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:3162323 | lifeskim:mentions | umls-concept:C0014563 | lld:lifeskim |
pubmed-article:3162323 | lifeskim:mentions | umls-concept:C2339371 | lld:lifeskim |
pubmed-article:3162323 | lifeskim:mentions | umls-concept:C0030685 | lld:lifeskim |
pubmed-article:3162323 | lifeskim:mentions | umls-concept:C0599702 | lld:lifeskim |
pubmed-article:3162323 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
pubmed-article:3162323 | lifeskim:mentions | umls-concept:C0680255 | lld:lifeskim |
pubmed-article:3162323 | lifeskim:mentions | umls-concept:C0391871 | lld:lifeskim |
pubmed-article:3162323 | lifeskim:mentions | umls-concept:C1283071 | lld:lifeskim |
pubmed-article:3162323 | lifeskim:mentions | umls-concept:C1963578 | lld:lifeskim |
pubmed-article:3162323 | lifeskim:mentions | umls-concept:C2349975 | lld:lifeskim |
pubmed-article:3162323 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:3162323 | pubmed:dateCreated | 1988-4-19 | lld:pubmed |
pubmed-article:3162323 | pubmed:abstractText | The voltage dependence of the intracellular Ca2+ transients was measured in single rat ventricular myocytes with the fluorescent Ca2+ indicator dye fura-2. The whole-cell voltage clamp technique was used to measure the membrane current, and 0.9 mM fura-2 was loaded into the cell by including it in the dialyzing solution of the patch electrode. A mechanical light chopper operating at 1200 Hz was used to obtain simultaneous measurements of the intracellular Ca2+ activity with fluorescence excitation on either side of the isosbestic point (330 nm and 410 nm). The symmetry of the two optical Ca2+ signals was used as a criterion to guard against artifacts resulting, for instance, from motion. The voltage dependence of peak Ca2+ current and the Ca2+ transient measured 25 ms after depolarizing clamps from a holding potential of -40 mV were bell-shaped and virtually identical. The Ca2+ entry estimated from the integral of the Ca2+ current (0 mV, 25 ms) corresponds to a 5-10 microM increase in the total intracellular Ca2+ concentration, whereas the optical signal indicated a 100 microM increase in total intracellular Ca2+. Repolarization of clamp pulses from highly positive potentials were accompanied by a second Ca2+ transient, the magnitude of which, when summed with that measured during depolarization, was nearly constant. Ryanodine (10 microM) had little or no effect on the peak Ca2+ current but reduced the magnitude of the early Ca2+ transients by 70-90%. Epinephrine (1 microM) increased the Ca2+ current and the Ca2+ transients, accelerated the rate of decline of the Ca2+ transients at potentials between -30 and +70 mV, and reduced the intracellular [Ca2+] below baseline at potentials positive to +80 or negative to -40 mV, where clamp pulses did not elicit any Ca2+ release. Elevation of intracellular cAMP mimicked the relaxant effect of epinephrine at depolarizing potentials, whereas elevation of extracellular [Ca2+] did not. These results suggest that most of the activator Ca2+ in rat ventricular cells is released from the sarcoplasmic reticulum as a graded response to sarcolemmal Ca2+ influx. Consistent with a graded Ca2+-induced Ca2+ release we find that epinephrine increases the internal Ca2+ release by increasing the Ca2+ current. Epinephrine may also increase the Ca2+ content of the sarcoplasmic reticulum that may, in turn, increase the Ca2+-induced Ca2+ release. The relaxant effect of epinephrine appears to be caused by enhanced rate of Ca2+ resequestration and is mediated by adenylate cyclase system. | lld:pubmed |
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pubmed-article:3162323 | pubmed:language | eng | lld:pubmed |
pubmed-article:3162323 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:3162323 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:3162323 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:3162323 | pubmed:month | Mar | lld:pubmed |
pubmed-article:3162323 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:3162323 | pubmed:author | pubmed-author:MoradMM | lld:pubmed |
pubmed-article:3162323 | pubmed:author | pubmed-author:CleemannLL | lld:pubmed |
pubmed-article:3162323 | pubmed:author | pubmed-author:CallewaertGG | lld:pubmed |
pubmed-article:3162323 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:3162323 | pubmed:volume | 85 | lld:pubmed |
pubmed-article:3162323 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:3162323 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:3162323 | pubmed:pagination | 2009-13 | lld:pubmed |
pubmed-article:3162323 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:3162323 | pubmed:meshHeading | pubmed-meshheading:3162323-... | lld:pubmed |
pubmed-article:3162323 | pubmed:year | 1988 | lld:pubmed |
pubmed-article:3162323 | pubmed:articleTitle | Epinephrine enhances Ca2+ current-regulated Ca2+ release and Ca2+ reuptake in rat ventricular myocytes. | lld:pubmed |
pubmed-article:3162323 | pubmed:affiliation | Department of Physiology, University of Pennsylvania, Philadelphia 19104. | lld:pubmed |
pubmed-article:3162323 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:3162323 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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