1. In muscle, intracellular calcium concentration, hence skeletal
muscle force and cardiac output, is regulated by uptake and release
of calcium from the sarcoplasmic reticulum (SR). The ryanodine receptor
(RyR) forms the calcium release channel in the SR. 2. Calcium release
through RyRs is modulated by a wide variety of endogenous molecules,
including small diffusible ligands such as ATP, Ca$^2+$ and Mg2+.
The regulation of RyR channels by ATP, Ca$^2+$ and Mg2+ is a
complex interplay of several regulatory mechanisms, which are still
being unravelled. Consequently, it is not clearly known how RyRs
are regulated in resting muscle and during contraction. 3. The present
paper reviews factors controlling the activity of RyRs in skeletal
and cardiac muscle with an emphasis on mechanistic insights derived
from single channel recording methods. 4. In addition, the nature
of dihydropyridine receptor (DHPR) control of RyRs in skeletal muscle
derived from experiments with peptide fragments of the DHPR II-III
loop is reviewed. 5. Finally, recent experiments on coupled RyRs
in lipid bilayers and their potential for resolving the elusive mechanisms
controlling calcium release during cardiac contraction are discussed.
School of Biomedical Sciences, University of Newcastle and Hunter
Medical Research Institute, Callaghan, New South Wales, Australia.
derek.laver@newcastle.edu.au
%0 Journal Article
%1 Lave_2006_1107
%A Laver, D. R.
%D 2006
%J Clin. Exp. Pharmacol. Physiol.
%K Calcium Channel Muscle, Myocardium; Receptor Release Ryanodine Skeletal;
%N 11
%P 1107--1113
%R 10.1111/j.1440-1681.2006.04500.x
%T Regulation of ryanodine receptors from skeletal and cardiac muscle
during rest and excitation.
%U http://dx.doi.org/10.1111/j.1440-1681.2006.04500.x
%V 33
%X 1. In muscle, intracellular calcium concentration, hence skeletal
muscle force and cardiac output, is regulated by uptake and release
of calcium from the sarcoplasmic reticulum (SR). The ryanodine receptor
(RyR) forms the calcium release channel in the SR. 2. Calcium release
through RyRs is modulated by a wide variety of endogenous molecules,
including small diffusible ligands such as ATP, Ca$^2+$ and Mg2+.
The regulation of RyR channels by ATP, Ca$^2+$ and Mg2+ is a
complex interplay of several regulatory mechanisms, which are still
being unravelled. Consequently, it is not clearly known how RyRs
are regulated in resting muscle and during contraction. 3. The present
paper reviews factors controlling the activity of RyRs in skeletal
and cardiac muscle with an emphasis on mechanistic insights derived
from single channel recording methods. 4. In addition, the nature
of dihydropyridine receptor (DHPR) control of RyRs in skeletal muscle
derived from experiments with peptide fragments of the DHPR II-III
loop is reviewed. 5. Finally, recent experiments on coupled RyRs
in lipid bilayers and their potential for resolving the elusive mechanisms
controlling calcium release during cardiac contraction are discussed.
@article{Lave_2006_1107,
abstract = {1. In muscle, intracellular calcium concentration, hence skeletal
muscle force and cardiac output, is regulated by uptake and release
of calcium from the sarcoplasmic reticulum (SR). The ryanodine receptor
(RyR) forms the calcium release channel in the SR. 2. Calcium release
through RyRs is modulated by a wide variety of endogenous molecules,
including small diffusible ligands such as ATP, {C}a$^{2+}$ and Mg2+.
The regulation of RyR channels by ATP, {C}a$^{2+}$ and Mg2+ is a
complex interplay of several regulatory mechanisms, which are still
being unravelled. Consequently, it is not clearly known how RyRs
are regulated in resting muscle and during contraction. 3. The present
paper reviews factors controlling the activity of RyRs in skeletal
and cardiac muscle with an emphasis on mechanistic insights derived
from single channel recording methods. 4. In addition, the nature
of dihydropyridine receptor (DHPR) control of RyRs in skeletal muscle
derived from experiments with peptide fragments of the DHPR II-III
loop is reviewed. 5. Finally, recent experiments on coupled RyRs
in lipid bilayers and their potential for resolving the elusive mechanisms
controlling calcium release during cardiac contraction are discussed.},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Laver, D. R.},
biburl = {https://www.bibsonomy.org/bibtex/2c94ab9ef96520c1cd90400a9f4eac66a/hake},
description = {The whole bibliography file I use.},
doi = {10.1111/j.1440-1681.2006.04500.x},
file = {Lave_2006_1107.pdf:Lave_2006_1107.pdf:PDF},
institution = {School of Biomedical Sciences, University of Newcastle and Hunter
Medical Research Institute, Callaghan, New South Wales, Australia.
derek.laver@newcastle.edu.au},
interhash = {41682646e78a2746f0ccbb68926187cb},
intrahash = {c94ab9ef96520c1cd90400a9f4eac66a},
journal = {Clin. Exp. Pharmacol. Physiol.},
keywords = {Calcium Channel Muscle, Myocardium; Receptor Release Ryanodine Skeletal;},
month = Nov,
number = 11,
pages = {1107--1113},
pii = {CEP4500},
pmid = {17042923},
timestamp = {2009-06-03T11:21:19.000+0200},
title = {Regulation of ryanodine receptors from skeletal and cardiac muscle
during rest and excitation.},
url = {http://dx.doi.org/10.1111/j.1440-1681.2006.04500.x},
volume = 33,
year = 2006
}