Ca(2+) signaling in cells is largely governed by Ca(2+) diffusion
and Ca(2+) binding to mobile and stationary Ca(2+) buffers, including
organelles. To examine Ca(2+) signaling in cardiac atrial myocytes,
a mathematical model of Ca(2+) diffusion was developed which represents
several subcellular compartments, including a subsarcolemmal space
with restricted diffusion, a myofilament space, and the cytosol.
The model was used to quantitatively simulate experimental Ca(2+)
signals in terms of amplitude, time course, and spatial features.
For experimental reference data, L-type Ca(2+) currents were recorded
from atrial cells with the whole-cell voltage-clamp technique. Ca(2+)
signals were simultaneously imaged with the fluorescent Ca(2+) indicator
Fluo-3 and a laser-scanning confocal microscope. The simulations
indicate that in atrial myocytes lacking T-tubules, Ca(2+) movement
from the cell membrane to the center of the cells relies strongly
on the presence of mobile Ca(2+) buffers, particularly when the sarcoplasmic
reticulum is inhibited pharmacologically. Furthermore, during the
influx of Ca(2+) large and steep concentration gradients are predicted
between the cytosol and the submicroscopically narrow subsarcolemmal
space. In addition, the computations revealed that, despite its low
Ca(2+) affinity, ATP acts as a significant buffer and carrier for
Ca(2+), even at the modest elevations of Ca(2+)(i) reached during
influx of Ca(2+).
%0 Journal Article
%1 Mich_2002_3134
%A Michailova, Anushka
%A DelPrincipe, Franco
%A Egger, Marcel
%A Niggli, Ernst
%D 2002
%J Biophys J
%K Adenosine Animals; Atria, Buffers; Calcium Calcium, Cardiovascular; Cells, Chemical; Computer Confocal, Cultured; Diffusion; Fluorescence, Guinea Heart Membrane Microscopy, Models, Muscle Myocardium, Patch-Clamp Pigs; Potentials, Reticulum, Ryanodine, Sarcoplasmic Signaling, Simulation; Techniques; Thapsigargin, Triphosphate, cytology/drug drug effects/metabolism; effects/physiology; metabolism; methods; pharmacology pharmacology;
%N 6
%P 3134--3151
%R 10.1016/S0006-3495(02)75317-4
%T Spatiotemporal features of Ca2+ buffering and diffusion in atrial
cardiac myocytes with inhibited sarcoplasmic reticulum.
%U http://dx.doi.org/10.1016/S0006-3495(02)75317-4
%V 83
%X Ca(2+) signaling in cells is largely governed by Ca(2+) diffusion
and Ca(2+) binding to mobile and stationary Ca(2+) buffers, including
organelles. To examine Ca(2+) signaling in cardiac atrial myocytes,
a mathematical model of Ca(2+) diffusion was developed which represents
several subcellular compartments, including a subsarcolemmal space
with restricted diffusion, a myofilament space, and the cytosol.
The model was used to quantitatively simulate experimental Ca(2+)
signals in terms of amplitude, time course, and spatial features.
For experimental reference data, L-type Ca(2+) currents were recorded
from atrial cells with the whole-cell voltage-clamp technique. Ca(2+)
signals were simultaneously imaged with the fluorescent Ca(2+) indicator
Fluo-3 and a laser-scanning confocal microscope. The simulations
indicate that in atrial myocytes lacking T-tubules, Ca(2+) movement
from the cell membrane to the center of the cells relies strongly
on the presence of mobile Ca(2+) buffers, particularly when the sarcoplasmic
reticulum is inhibited pharmacologically. Furthermore, during the
influx of Ca(2+) large and steep concentration gradients are predicted
between the cytosol and the submicroscopically narrow subsarcolemmal
space. In addition, the computations revealed that, despite its low
Ca(2+) affinity, ATP acts as a significant buffer and carrier for
Ca(2+), even at the modest elevations of Ca(2+)(i) reached during
influx of Ca(2+).
@article{Mich_2002_3134,
abstract = {Ca(2+) signaling in cells is largely governed by Ca(2+) diffusion
and Ca(2+) binding to mobile and stationary Ca(2+) buffers, including
organelles. To examine Ca(2+) signaling in cardiac atrial myocytes,
a mathematical model of Ca(2+) diffusion was developed which represents
several subcellular compartments, including a subsarcolemmal space
with restricted diffusion, a myofilament space, and the cytosol.
The model was used to quantitatively simulate experimental Ca(2+)
signals in terms of amplitude, time course, and spatial features.
For experimental reference data, L-type Ca(2+) currents were recorded
from atrial cells with the whole-cell voltage-clamp technique. Ca(2+)
signals were simultaneously imaged with the fluorescent Ca(2+) indicator
Fluo-3 and a laser-scanning confocal microscope. The simulations
indicate that in atrial myocytes lacking T-tubules, Ca(2+) movement
from the cell membrane to the center of the cells relies strongly
on the presence of mobile Ca(2+) buffers, particularly when the sarcoplasmic
reticulum is inhibited pharmacologically. Furthermore, during the
influx of Ca(2+) large and steep concentration gradients are predicted
between the cytosol and the submicroscopically narrow subsarcolemmal
space. In addition, the computations revealed that, despite its low
Ca(2+) affinity, ATP acts as a significant buffer and carrier for
Ca(2+), even at the modest elevations of [Ca(2+)](i) reached during
influx of Ca(2+).},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Michailova, Anushka and DelPrincipe, Franco and Egger, Marcel and Niggli, Ernst},
biburl = {https://www.bibsonomy.org/bibtex/203cc0945809444a821efc6d1ebd28d73/hake},
description = {The whole bibliography file I use.},
doi = {10.1016/S0006-3495(02)75317-4},
institution = {Department of Physiology, University of Bern, Buehlplatz 5, CH-3012
Bern, Switzerland. niggli@pyl.unibe.ch},
interhash = {95c940c754fbce6aed39de42642b54ff},
intrahash = {03cc0945809444a821efc6d1ebd28d73},
journal = {Biophys J},
keywords = {Adenosine Animals; Atria, Buffers; Calcium Calcium, Cardiovascular; Cells, Chemical; Computer Confocal, Cultured; Diffusion; Fluorescence, Guinea Heart Membrane Microscopy, Models, Muscle Myocardium, Patch-Clamp Pigs; Potentials, Reticulum, Ryanodine, Sarcoplasmic Signaling, Simulation; Techniques; Thapsigargin, Triphosphate, cytology/drug drug effects/metabolism; effects/physiology; metabolism; methods; pharmacology pharmacology;},
month = Dec,
number = 6,
pages = {3134--3151},
pii = {S0006-3495(02)75317-4},
pmid = {12496084},
timestamp = {2009-06-03T11:21:23.000+0200},
title = {Spatiotemporal features of Ca2+ buffering and diffusion in atrial
cardiac myocytes with inhibited sarcoplasmic reticulum.},
url = {http://dx.doi.org/10.1016/S0006-3495(02)75317-4},
volume = 83,
year = 2002
}