Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1991-10-4
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)
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-1169758, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-13714849, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2158146, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2301565, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2309919, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2411919, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2419483, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2431095, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2440616, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2446391, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2451732, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2451806, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2467378, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2475607, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2543067, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2553859, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2580043, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2580044, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2627235, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2923192, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-2998207, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-3058361, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-3108033, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-3162323, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-3266079, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-3267019, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-3395664, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-3413129, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-3494101, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-3686010, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-3798114, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-3838314, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-384460, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-3981128, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-4275030, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-4537238, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-4540479, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-4797949, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-6096480, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-6283359, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-6314245, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-6346892, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-6655593, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-6758036, http://linkedlifedata.com/resource/pubmed/commentcorrection/1653321-957259
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-3751
pubmed:author
pubmed:issnType
Print
pubmed:volume
432
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
283-312
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Role of Ca2+ channel in cardiac excitation-contraction coupling in the rat: evidence from Ca2+ transients and contraction.
pubmed:affiliation
Department of Physiology, University of Pennsylvania, Philadelphia 19104-6085.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't