pubmed-article:1653321 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1653321 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:1653321 | lifeskim:mentions | umls-concept:C0040704 | lld:lifeskim |
pubmed-article:1653321 | lifeskim:mentions | umls-concept:C0687129 | lld:lifeskim |
pubmed-article:1653321 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
pubmed-article:1653321 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:1653321 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
pubmed-article:1653321 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
pubmed-article:1653321 | lifeskim:mentions | umls-concept:C1948027 | lld:lifeskim |
pubmed-article:1653321 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
pubmed-article:1653321 | lifeskim:mentions | umls-concept:C0332120 | lld:lifeskim |
pubmed-article:1653321 | lifeskim:mentions | umls-concept:C1140999 | lld:lifeskim |
pubmed-article:1653321 | pubmed:dateCreated | 1991-10-4 | lld:pubmed |
pubmed-article:1653321 | pubmed:abstractText | 1. Optical methods were used to measure simultaneously unloaded cell shortening and intracellular Ca2+ transients in whole-cell voltage clamped rat ventricular myocytes. Red light (greater than 670 nm) was used to measure cell shortening with a linear photodiode array. The dyes Fura-2 (Kd = 140 nM) and Mag-Fura-2 (Kd = 44 microM) were used as Ca2+ indicators with fluorescence excitation at 340 and 410 nm and emission at 510 nm. 2. Repeated measurements at 6 s intervals as 0.4 mM-Fura-2 diffused into the cell from the tip of the voltage clamp pipette showed no decrease in the rate of rise and peak value of the intracellular Ca2+ transient and only a small suppression of cell shortening, suggesting that the molecular mechanisms regulating the Ca2+ release were not significantly altered by the buffering capacity of the Fura-2. 3. Experiments in which the sarcoplasmic reticulum (SR) was depleted of Ca2+ either by exposure to caffeine or by repeated brief (20 ms) voltage clamp depolarizations confirm that the SR is the major source of activator Ca2+. 4. Mag-Fura-2 (1 or 5 mM) was used to register the initial rapid development of the [Ca2+]i transient but the later time course of the Ca2+ transients measured with this dye was obscured by motion artifacts resulting from cell shortening. 5. Both Fura-2 and Mag-Fura-2 showed that depolarization to 0 mV from a holding potential of -80 mV resulted in a [Ca2+]i transient which developed with a delay of 3-9 ms and approached its peak value in an additional 8-19 ms. Both Ca2+ indicators also showed that the Ca2+ transient approached its peak value more slowly as the clamped membrane potential was made increasingly more positive. 6. The voltage dependencies of the Ca2+ signal (Fura-2) and cell shortening were both bell-shaped and were qualitatively similar to the voltage dependence of Ca2+ current simultaneously measured. This was observed with holding potentials of both -40 and -80 mV. 7. Comparison of the temporal relation of the Ca2+ current, ICa, and intracellular Ca2+ transient (Fura-2) and cell shortening at different membrane potentials showed that Ca2+ transient measured 25 ms into the depolarization correlated closely to the integral of the Ca2+ current measured prior to this time. Cell shortening, on the other hand, peaked about 100 ms later and correlated with measurements of the Ca2+ activity at the later time.(ABSTRACT TRUNCATED AT 400 WORDS) | lld:pubmed |
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pubmed-article:1653321 | pubmed:language | eng | lld:pubmed |
pubmed-article:1653321 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1653321 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:1653321 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1653321 | pubmed:month | Jan | lld:pubmed |
pubmed-article:1653321 | pubmed:issn | 0022-3751 | lld:pubmed |
pubmed-article:1653321 | pubmed:author | pubmed-author:MoradMM | lld:pubmed |
pubmed-article:1653321 | pubmed:author | pubmed-author:CleemannLL | lld:pubmed |
pubmed-article:1653321 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1653321 | pubmed:volume | 432 | lld:pubmed |
pubmed-article:1653321 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1653321 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1653321 | pubmed:pagination | 283-312 | lld:pubmed |
pubmed-article:1653321 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:1653321 | pubmed:year | 1991 | lld:pubmed |
pubmed-article:1653321 | pubmed:articleTitle | Role of Ca2+ channel in cardiac excitation-contraction coupling in the rat: evidence from Ca2+ transients and contraction. | lld:pubmed |
pubmed-article:1653321 | pubmed:affiliation | Department of Physiology, University of Pennsylvania, Philadelphia 19104-6085. | lld:pubmed |
pubmed-article:1653321 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1653321 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:1653321 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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