Our aim was to measure the influence of sarcoplasmic reticulum (SR)
calcium content (Ca(SRT)) and free SR Ca (Ca(SR)) on the
fraction of SR calcium released during voltage clamp steps in isolated
rabbit ventricular myocytes. Ca(SRT), as measured by caffeine
application, was progressively increased by conditioning pulses.
Sodium was absent in both the intracellular and in the extracellular
solutions to block sodium/calcium exchange. Total cytosolic calcium
flux during the transient was inferred from I(Ca), Ca(SRT), Ca(i),
and cellular buffering characteristics. Fluxes via the calcium current
(I(Ca)), the SR calcium pump, and passive leak from the SR were evaluated
to determine SR calcium release flux (J(rel)). Excitation-contraction
(EC) coupling was characterized with respect to both gain (integral
J(rel)/integral I(Ca)) and fractional SR calcium release. Both parameters
were virtually zero for a small, but measurable Ca(SRT). Gain
and fractional SR calcium release increased steeply and nonlinearly
with both Ca(SRT) and Ca(SR). We conclude that potentiation
of EC coupling can be correlated with both Ca(SRT) and Ca(SR).
While fractional SR calcium release was not linearly dependent upon
Ca(SR), intra-SR calcium may play a crucial role in regulating
the SR calcium release process.
%0 Journal Article
%1 Shan_2000_334
%A Shannon, T. R.
%A Ginsburg, K. S.
%A Bers, D. M.
%D 2000
%J Biophys. J.
%K 10620297 AMP-Dependent ATPase, Action Activation, Adenosine Adrenergic Allosteric Animals, Binding, Biological Biological, Caffeine, Calcium Calcium, Calcium-Binding Cardiac, Cardiovascular, Catalytic Cell Cells, Channels, Computer Congestive, Contraction, Cultured, Cyclic Cytosol, Diastole, Dogs, Domain, Electric Enzyme Exchanger, Factors, Failure, Ferrets, Fibers, Gov't, Heart Heart, Humans, Hydrolysis, Inhibitors, Intracellular Ion Isoproterenol, Kinases, Kinetics, Knockout, Membrane Membrane, Membranes, Mice, Microsomes, Models, Muscle Mutagenesis, Myocardial Myocardium, Myocytes, Nickel, Non-U.S. P.H.S., Patch-Clamp Phosphorylation, Potentials, Protein Proteins, Rabbits, Red, Regulation, Research Reticulum, Ruthenium Sarcoplasmic Signaling, Simulation, Sodium-Calcium Stimulation, Support, Techniques, Tetracaine, Thapsigargin, Thermodynamics, Time Transport, Triphosphate, U.S. Ventricles, beta-Agonists, {C}a$^{2+}$-Transporting
%N 1
%P 334--343
%T Potentiation of fractional sarcoplasmic reticulum calcium release
by total and free intra-sarcoplasmic reticulum calcium concentration.
%U http://www.biophysj.org/cgi/content/full/78/1/334
%V 78
%X Our aim was to measure the influence of sarcoplasmic reticulum (SR)
calcium content (Ca(SRT)) and free SR Ca (Ca(SR)) on the
fraction of SR calcium released during voltage clamp steps in isolated
rabbit ventricular myocytes. Ca(SRT), as measured by caffeine
application, was progressively increased by conditioning pulses.
Sodium was absent in both the intracellular and in the extracellular
solutions to block sodium/calcium exchange. Total cytosolic calcium
flux during the transient was inferred from I(Ca), Ca(SRT), Ca(i),
and cellular buffering characteristics. Fluxes via the calcium current
(I(Ca)), the SR calcium pump, and passive leak from the SR were evaluated
to determine SR calcium release flux (J(rel)). Excitation-contraction
(EC) coupling was characterized with respect to both gain (integral
J(rel)/integral I(Ca)) and fractional SR calcium release. Both parameters
were virtually zero for a small, but measurable Ca(SRT). Gain
and fractional SR calcium release increased steeply and nonlinearly
with both Ca(SRT) and Ca(SR). We conclude that potentiation
of EC coupling can be correlated with both Ca(SRT) and Ca(SR).
While fractional SR calcium release was not linearly dependent upon
Ca(SR), intra-SR calcium may play a crucial role in regulating
the SR calcium release process.
@article{Shan_2000_334,
abstract = {Our aim was to measure the influence of sarcoplasmic reticulum (SR)
calcium content ([Ca]({SRT})) and free SR [Ca] ([Ca](SR)) on the
fraction of SR calcium released during voltage clamp steps in isolated
rabbit ventricular myocytes. [Ca]({SRT}), as measured by caffeine
application, was progressively increased by conditioning pulses.
Sodium was absent in both the intracellular and in the extracellular
solutions to block sodium/calcium exchange. Total cytosolic calcium
flux during the transient was inferred from I(Ca), [Ca]({SRT}), [Ca](i),
and cellular buffering characteristics. Fluxes via the calcium current
(I(Ca)), the SR calcium pump, and passive leak from the SR were evaluated
to determine SR calcium release flux (J(rel)). Excitation-contraction
(EC) coupling was characterized with respect to both gain (integral
J(rel)/integral I(Ca)) and fractional SR calcium release. Both parameters
were virtually zero for a small, but measurable [Ca]({SRT}). Gain
and fractional SR calcium release increased steeply and nonlinearly
with both [Ca]({SRT}) and [Ca](SR). We conclude that potentiation
of EC coupling can be correlated with both [Ca]({SRT}) and [Ca](SR).
While fractional SR calcium release was not linearly dependent upon
[Ca](SR), intra-SR calcium may play a crucial role in regulating
the SR calcium release process.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Shannon, T. R. and Ginsburg, K. S. and Bers, D. M.},
biburl = {https://www.bibsonomy.org/bibtex/22d07c293fa17a0469f3ca9521e4d0f99/hake},
description = {The whole bibliography file I use.},
file = {Shan_2000_334.pdf:Shan_2000_334.pdf:PDF},
interhash = {bed090769960f0ac6df3fcf4aeefb0e1},
intrahash = {2d07c293fa17a0469f3ca9521e4d0f99},
journal = {Biophys. J.},
key = 102,
keywords = {10620297 AMP-Dependent ATPase, Action Activation, Adenosine Adrenergic Allosteric Animals, Binding, Biological Biological, Caffeine, Calcium Calcium, Calcium-Binding Cardiac, Cardiovascular, Catalytic Cell Cells, Channels, Computer Congestive, Contraction, Cultured, Cyclic Cytosol, Diastole, Dogs, Domain, Electric Enzyme Exchanger, Factors, Failure, Ferrets, Fibers, Gov't, Heart Heart, Humans, Hydrolysis, Inhibitors, Intracellular Ion Isoproterenol, Kinases, Kinetics, Knockout, Membrane Membrane, Membranes, Mice, Microsomes, Models, Muscle Mutagenesis, Myocardial Myocardium, Myocytes, Nickel, Non-U.S. P.H.S., Patch-Clamp Phosphorylation, Potentials, Protein Proteins, Rabbits, Red, Regulation, Research Reticulum, Ruthenium Sarcoplasmic Signaling, Simulation, Sodium-Calcium Stimulation, Support, Techniques, Tetracaine, Thapsigargin, Thermodynamics, Time Transport, Triphosphate, U.S. Ventricles, beta-Agonists, {C}a$^{2+}$-Transporting},
month = Jan,
number = 1,
pages = {334--343},
pmid = {10620297},
timestamp = {2009-06-03T11:21:29.000+0200},
title = {Potentiation of fractional sarcoplasmic reticulum calcium release
by total and free intra-sarcoplasmic reticulum calcium concentration.},
url = {http://www.biophysj.org/cgi/content/full/78/1/334},
volume = 78,
year = 2000
}