The amount of Ca$^2+$ released from the sarcoplasmic reticulum
(SR) is a principal determinant of cardiac contractility. Normally,
the SR Ca$^2+$ stores are mobilized through the mechanism of
Ca$^2+$-induced Ca$^2+$ release (CICR). In this process,
Ca$^2+$ enters the cell through plasmalemmal voltage-dependent
Ca$^2+$ channels to activate the Ca$^2+$ release channels
in the SR membrane. Consequently, the control of Ca$^2+$ release
by cytosolic Ca$^2+$ has traditionally been the main focus of
cardiac excitation-contraction (EC) coupling research. Evidence obtained
recently suggests that SR Ca release is controlled not only by cytosolic
Ca$^2+$, but also by Ca$^2+$ in the lumen of the SR. The
presence of a luminal Ca$^2+$ sensor regulating release of SR
luminal Ca$^2+$ potentially has profound implications for our
understanding of EC coupling and intracellular Ca$^2+$ cycling.
Here we review evidence, obtained using in situ and in vitro approaches,
in support of such a luminal Ca$^2+$ sensor in cardiac muscle.
We also discuss the role of control of Ca$^2+$ release channels
by luminal Ca$^2+$ in termination and stabilization of CICR,
as well as in shaping the response of cardiac myocytes to various
inotropic influences and diseased states such as Ca$^2+$ overload
and heart failure.
%0 Journal Article
%1 Gyoer_2002_d1454
%A Gy�rke, Sandor
%A Gy�rke, Inna
%A Lukyanenko, Valeriy
%A Terentyev, Dmitriy
%A Viatchenko-Karpinski, Serge
%A Wiesner, Theodore F
%D 2002
%J Front Biosci
%K 12045014 Animals, Calcium Calcium, Channels, Gov't, Heart, Humans, Myocardium, Non-U.S. P.H.S., Research Reticulum, Sarcoplasmic Support, U.S.
%P d1454--d1463
%T Regulation of sarcoplasmic reticulum calcium release by luminal calcium
in cardiac muscle.
%U http://www.bioscience.org/2002/v7/d/gyorke/list.htm
%V 7
%X The amount of Ca$^2+$ released from the sarcoplasmic reticulum
(SR) is a principal determinant of cardiac contractility. Normally,
the SR Ca$^2+$ stores are mobilized through the mechanism of
Ca$^2+$-induced Ca$^2+$ release (CICR). In this process,
Ca$^2+$ enters the cell through plasmalemmal voltage-dependent
Ca$^2+$ channels to activate the Ca$^2+$ release channels
in the SR membrane. Consequently, the control of Ca$^2+$ release
by cytosolic Ca$^2+$ has traditionally been the main focus of
cardiac excitation-contraction (EC) coupling research. Evidence obtained
recently suggests that SR Ca release is controlled not only by cytosolic
Ca$^2+$, but also by Ca$^2+$ in the lumen of the SR. The
presence of a luminal Ca$^2+$ sensor regulating release of SR
luminal Ca$^2+$ potentially has profound implications for our
understanding of EC coupling and intracellular Ca$^2+$ cycling.
Here we review evidence, obtained using in situ and in vitro approaches,
in support of such a luminal Ca$^2+$ sensor in cardiac muscle.
We also discuss the role of control of Ca$^2+$ release channels
by luminal Ca$^2+$ in termination and stabilization of CICR,
as well as in shaping the response of cardiac myocytes to various
inotropic influences and diseased states such as Ca$^2+$ overload
and heart failure.
@article{Gyoer_2002_d1454,
abstract = {The amount of {C}a$^{2+}$ released from the sarcoplasmic reticulum
(SR) is a principal determinant of cardiac contractility. Normally,
the SR {C}a$^{2+}$ stores are mobilized through the mechanism of
{C}a$^{2+}$-induced {C}a$^{2+}$ release (CICR). In this process,
{C}a$^{2+}$ enters the cell through plasmalemmal voltage-dependent
{C}a$^{2+}$ channels to activate the {C}a$^{2+}$ release channels
in the SR membrane. Consequently, the control of {C}a$^{2+}$ release
by cytosolic {C}a$^{2+}$ has traditionally been the main focus of
cardiac excitation-contraction (EC) coupling research. Evidence obtained
recently suggests that SR Ca release is controlled not only by cytosolic
{C}a$^{2+}$, but also by {C}a$^{2+}$ in the lumen of the SR. The
presence of a luminal {C}a$^{2+}$ sensor regulating release of SR
luminal {C}a$^{2+}$ potentially has profound implications for our
understanding of EC coupling and intracellular {C}a$^{2+}$ cycling.
Here we review evidence, obtained using in situ and in vitro approaches,
in support of such a luminal {C}a$^{2+}$ sensor in cardiac muscle.
We also discuss the role of control of {C}a$^{2+}$ release channels
by luminal {C}a$^{2+}$ in termination and stabilization of CICR,
as well as in shaping the response of cardiac myocytes to various
inotropic influences and diseased states such as {C}a$^{2+}$ overload
and heart failure.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Gy�rke, Sandor and Gy�rke, Inna and Lukyanenko, Valeriy and Terentyev, Dmitriy and Viatchenko-Karpinski, Serge and Wiesner, Theodore F},
biburl = {https://www.bibsonomy.org/bibtex/21e4fe61ff5e8aa45d23a0b54579084fc/hake},
description = {The whole bibliography file I use.},
file = {Gyoer_2002_d1454.pdf:Gyoer_2002_d1454.pdf:PDF},
interhash = {e91512e22a5a73d48b7b2f673dbc04be},
intrahash = {1e4fe61ff5e8aa45d23a0b54579084fc},
journal = {Front Biosci},
key = 190,
keywords = {12045014 Animals, Calcium Calcium, Channels, Gov't, Heart, Humans, Myocardium, Non-U.S. P.H.S., Research Reticulum, Sarcoplasmic Support, U.S.},
month = Jun,
pages = {d1454--d1463},
pmid = {12045014},
timestamp = {2009-06-03T11:21:13.000+0200},
title = {Regulation of sarcoplasmic reticulum calcium release by luminal calcium
in cardiac muscle.},
url = {http://www.bioscience.org/2002/v7/d/gyorke/list.htm},
volume = 7,
year = 2002
}