Calcium-induced release of calcium from the cardiac sarcoplasmic
reticulum.
A. Fabiato. Am. J. Physiol., 245 (1):
C1--14(July 1983)
Abstract
The hypothesis of a Ca$^2+$-induced Ca$^2+$ release (CICR)
from the sarcoplasmic reticulum (SR) is supported by experiments
done in skinned cardiac cells (sarcolemma removed by microdissection).
According to this hypothesis, the transsarcolemmal Ca$^2+$ influx
does not activate the myofilaments directly but through the induction
of a Ca$^2+$ release from the SR. The stimulus gating CICR is
not a small change in free Ca$^2+$ concentration (deltafree
Ca$^2+$) outside the SR but a function of the rate of this change
(deltafree Ca$^2+$/delta t). The initial relatively fast component
of the transsarcolemmal Ca$^2+$ current would trigger Ca$^2+$
release; the subsequent slow component, perhaps corresponding to
noninactivating Ca$^2+$ channels, would load the SR with an amount
of Ca$^2+$ available for release during subsequent beats. Inactivation
of CICR is caused by the large increase of free Ca$^2+$ outside
the SR resulting from Ca$^2+$ release, which inhibits further
release. This negative feedback helps to explain that CICR is not
all or none. During relaxation the Ca$^2+$ reaccumulation in
the SR is backed up by the Ca$^2+$ efflux across the sarcolemma
through Na$^+$-Ca$^2+$ exchange and the sarcolemmal Ca$^2+$
pump. Computations of the Ca$^2+$ buffering in the mammalian
ventricular cell and of the systolic transsarcolemmal Ca$^2+$
influx do not support the alternative hypothesis that this influx
of Ca$^2+$ is large enough to activate the myofilaments directly.
Yet the hypothesis of a CICR can be challenged because of many problems
and uncertainties related to the preparations and methods used for
skinned cardiac cell experiments.
%0 Journal Article
%1 Fabi_1983_C1
%A Fabiato, A.
%D 1983
%J Am. J. Physiol.
%K 15475522 Adenosine Animals, Caffeine, Calcium, Calmodulin, Cell Compartmentation, Electron, Feedback, Gov't, Guinea Heart Heart, Liver, Male, Microscopy, Myocardium, Non-U.S. P.H.S., Permeability, Phosphorylases, Pigs, Potassium, Ranidae, Research Reticulum, Saponins, Sarcolemma, Sarcoplasmic Sodium, Support, Triphosphate, U.S. Ventricles,
%N 1
%P C1--14
%T Calcium-induced release of calcium from the cardiac sarcoplasmic
reticulum.
%V 245
%X The hypothesis of a Ca$^2+$-induced Ca$^2+$ release (CICR)
from the sarcoplasmic reticulum (SR) is supported by experiments
done in skinned cardiac cells (sarcolemma removed by microdissection).
According to this hypothesis, the transsarcolemmal Ca$^2+$ influx
does not activate the myofilaments directly but through the induction
of a Ca$^2+$ release from the SR. The stimulus gating CICR is
not a small change in free Ca$^2+$ concentration (deltafree
Ca$^2+$) outside the SR but a function of the rate of this change
(deltafree Ca$^2+$/delta t). The initial relatively fast component
of the transsarcolemmal Ca$^2+$ current would trigger Ca$^2+$
release; the subsequent slow component, perhaps corresponding to
noninactivating Ca$^2+$ channels, would load the SR with an amount
of Ca$^2+$ available for release during subsequent beats. Inactivation
of CICR is caused by the large increase of free Ca$^2+$ outside
the SR resulting from Ca$^2+$ release, which inhibits further
release. This negative feedback helps to explain that CICR is not
all or none. During relaxation the Ca$^2+$ reaccumulation in
the SR is backed up by the Ca$^2+$ efflux across the sarcolemma
through Na$^+$-Ca$^2+$ exchange and the sarcolemmal Ca$^2+$
pump. Computations of the Ca$^2+$ buffering in the mammalian
ventricular cell and of the systolic transsarcolemmal Ca$^2+$
influx do not support the alternative hypothesis that this influx
of Ca$^2+$ is large enough to activate the myofilaments directly.
Yet the hypothesis of a CICR can be challenged because of many problems
and uncertainties related to the preparations and methods used for
skinned cardiac cell experiments.
@article{Fabi_1983_C1,
abstract = {The hypothesis of a {C}a$^{2+}$-induced {C}a$^{2+}$ release (CICR)
from the sarcoplasmic reticulum (SR) is supported by experiments
done in skinned cardiac cells (sarcolemma removed by microdissection).
According to this hypothesis, the transsarcolemmal {C}a$^{2+}$ influx
does not activate the myofilaments directly but through the induction
of a {C}a$^{2+}$ release from the SR. The stimulus gating CICR is
not a small change in free {C}a$^{2+}$ concentration (delta[free
{C}a$^{2+}$]) outside the SR but a function of the rate of this change
(delta[free {C}a$^{2+}$/delta t]). The initial relatively fast component
of the transsarcolemmal {C}a$^{2+}$ current would trigger {C}a$^{2+}$
release; the subsequent slow component, perhaps corresponding to
noninactivating {C}a$^{2+}$ channels, would load the SR with an amount
of {C}a$^{2+}$ available for release during subsequent beats. Inactivation
of CICR is caused by the large increase of [free {C}a$^{2+}$] outside
the SR resulting from {C}a$^{2+}$ release, which inhibits further
release. This negative feedback helps to explain that CICR is not
all or none. During relaxation the {C}a$^{2+}$ reaccumulation in
the SR is backed up by the {C}a$^{2+}$ efflux across the sarcolemma
through {N}a$^{+}$-{C}a$^{2+}$ exchange and the sarcolemmal {C}a$^{2+}$
pump. Computations of the {C}a$^{2+}$ buffering in the mammalian
ventricular cell and of the systolic transsarcolemmal {C}a$^{2+}$
influx do not support the alternative hypothesis that this influx
of {C}a$^{2+}$ is large enough to activate the myofilaments directly.
Yet the hypothesis of a CICR can be challenged because of many problems
and uncertainties related to the preparations and methods used for
skinned cardiac cell experiments.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Fabiato, A.},
biburl = {https://www.bibsonomy.org/bibtex/282ccfaea7a18bec3564588d1d91551e3/hake},
description = {The whole bibliography file I use.},
file = {Fabi_1983_C1.pdf:Fabi_1983_C1.pdf:PDF},
interhash = {0d648e0d48706a651c05f21d81a567ca},
intrahash = {82ccfaea7a18bec3564588d1d91551e3},
journal = {Am. J. Physiol.},
keywords = {15475522 Adenosine Animals, Caffeine, Calcium, Calmodulin, Cell Compartmentation, Electron, Feedback, Gov't, Guinea Heart Heart, Liver, Male, Microscopy, Myocardium, Non-U.S. P.H.S., Permeability, Phosphorylases, Pigs, Potassium, Ranidae, Research Reticulum, Saponins, Sarcolemma, Sarcoplasmic Sodium, Support, Triphosphate, U.S. Ventricles,},
month = Jul,
number = 1,
pages = {C1--14},
pmid = {15475522},
timestamp = {2009-06-03T11:21:11.000+0200},
title = {Calcium-induced release of calcium from the cardiac sarcoplasmic
reticulum.},
volume = 245,
year = 1983
}