Free Ca$^2+$ inside the sarcoplasmic reticulum (Ca$^2+$SR)
is difficult to measure yet critically important in controlling many
cellular systems. In cardiac myocytes, Ca$^2+$SR regulates
cardiac contractility. We directly measure Ca$^2+$SR in intact
cardiac myocytes dynamically and quantitatively during beats, with
high spatial resolution. Diastolic Ca$^2+$SR (1 to 1.5 mmol/L)
is only partially depleted (24\% to 63\%) during contraction. There
is little temporal delay in the decline in Ca$^2+$SR at release
junctions and between junctions, indicating rapid internal diffusion.
The incomplete local Ca$^2+$ release shows that the inherently
positive feedback of Ca$^2+$-induced Ca$^2+$ release terminates,
despite a large residual driving force. These findings place stringent
novel constraints on how excitation-contraction coupling works in
heart and also reveal a Ca$^2+$ store reserve that could in principle
be a therapeutic target to enhance cardiac function in heart failure.
%0 Journal Article
%1 Shan_2003_40
%A Shannon, Thomas R
%A Guo, Tao
%A Bers, Donald M
%D 2003
%J Circ. Res.
%K 12855669 Action Adrenergic Animals, Caffeine, Calcium Calcium, Cardiac, Cardiovascular, Cell Cells, Computer Congestive, Contraction, Cultured, Cytosol, Electric Failure, Gov't, Heart Humans, Ion Isoproterenol, Membrane Membrane, Models, Myocardial Myocardium, Myocytes, Non-U.S. P.H.S., Potentials, Rabbits, Research Reticulum, Sarcoplasmic Signaling, Simulation, Stimulation, Support, Tetracaine, Transport, U.S. Ventricles, beta-Agonists,
%N 1
%P 40--45
%R 10.1161/01.RES.0000079967.11815.19
%T Ca$^2+$ scraps: local depletions of free Ca$^2+$ in cardiac
sarcoplasmic reticulum during contractions leave substantial Ca$^2+$
reserve.
%U http://dx.doi.org/10.1161/01.RES.0000079967.11815.19
%V 93
%X Free Ca$^2+$ inside the sarcoplasmic reticulum (Ca$^2+$SR)
is difficult to measure yet critically important in controlling many
cellular systems. In cardiac myocytes, Ca$^2+$SR regulates
cardiac contractility. We directly measure Ca$^2+$SR in intact
cardiac myocytes dynamically and quantitatively during beats, with
high spatial resolution. Diastolic Ca$^2+$SR (1 to 1.5 mmol/L)
is only partially depleted (24\% to 63\%) during contraction. There
is little temporal delay in the decline in Ca$^2+$SR at release
junctions and between junctions, indicating rapid internal diffusion.
The incomplete local Ca$^2+$ release shows that the inherently
positive feedback of Ca$^2+$-induced Ca$^2+$ release terminates,
despite a large residual driving force. These findings place stringent
novel constraints on how excitation-contraction coupling works in
heart and also reveal a Ca$^2+$ store reserve that could in principle
be a therapeutic target to enhance cardiac function in heart failure.
@article{Shan_2003_40,
abstract = {Free [{C}a$^{2+}$] inside the sarcoplasmic reticulum ([{C}a$^{2+}$]SR)
is difficult to measure yet critically important in controlling many
cellular systems. In cardiac myocytes, [{C}a$^{2+}$]SR regulates
cardiac contractility. We directly measure [{C}a$^{2+}$]SR in intact
cardiac myocytes dynamically and quantitatively during beats, with
high spatial resolution. Diastolic [{C}a$^{2+}$]SR (1 to 1.5 mmol/L)
is only partially depleted (24\% to 63\%) during contraction. There
is little temporal delay in the decline in [{C}a$^{2+}$]SR at release
junctions and between junctions, indicating rapid internal diffusion.
The incomplete local {C}a$^{2+}$ release shows that the inherently
positive feedback of {C}a$^{2+}$-induced {C}a$^{2+}$ release terminates,
despite a large residual driving force. These findings place stringent
novel constraints on how excitation-contraction coupling works in
heart and also reveal a {C}a$^{2+}$ store reserve that could in principle
be a therapeutic target to enhance cardiac function in heart failure.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Shannon, Thomas R and Guo, Tao and Bers, Donald M},
biburl = {https://www.bibsonomy.org/bibtex/2afc555ae55836a4f2d405831003a81a0/hake},
description = {The whole bibliography file I use.},
doi = {10.1161/01.RES.0000079967.11815.19},
file = {Shan_2003_40.pdf:Shan_2003_40.pdf:PDF},
interhash = {2135efc466c7a91a4c9e529792facff2},
intrahash = {afc555ae55836a4f2d405831003a81a0},
journal = {Circ. Res.},
key = 105,
keywords = {12855669 Action Adrenergic Animals, Caffeine, Calcium Calcium, Cardiac, Cardiovascular, Cell Cells, Computer Congestive, Contraction, Cultured, Cytosol, Electric Failure, Gov't, Heart Humans, Ion Isoproterenol, Membrane Membrane, Models, Myocardial Myocardium, Myocytes, Non-U.S. P.H.S., Potentials, Rabbits, Research Reticulum, Sarcoplasmic Signaling, Simulation, Stimulation, Support, Tetracaine, Transport, U.S. Ventricles, beta-Agonists,},
month = Jul,
number = 1,
pages = {40--45},
pii = {01.RES.0000079967.11815.19},
pmid = {12855669},
timestamp = {2009-06-03T11:21:30.000+0200},
title = {{C}a$^{2+}$ scraps: local depletions of free [{C}a$^{2+}$] in cardiac
sarcoplasmic reticulum during contractions leave substantial {C}a$^{2+}$
reserve.},
url = {http://dx.doi.org/10.1161/01.RES.0000079967.11815.19},
volume = 93,
year = 2003
}