Crosstalk between Mitochondrial and Sarcoplasmic Reticulum Ca2+ Cycling Modulates Cardiac Pacemaker Cell Automaticity

Mitochondria dynamically buffer cytosolic Ca(2+) in cardiac ventricular cells and this affects the Ca(2+) load of the sarcoplasmic reticulum (SR). In sinoatrial-node cells (SANC) the SR generates periodic local, subsarcolemmal Ca(2+) releases (LCRs) that depend upon the SR load and are involved in S...

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Veröffentlicht in:	PloS one Jg. 7; H. 5; S. e37582
Hauptverfasser:	Yaniv, Yael, Spurgeon, Harold A., Lyashkov, Alexey E., Yang, Dongmei, Ziman, Bruce D., Maltsev, Victor A., Lakatta, Edward G.
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States Public Library of Science 29.05.2012 Public Library of Science (PLoS)
Schlagworte:	Action potential Action Potentials - drug effects Aging Animals Automation Biology Calcium (mitochondrial) Calcium (reticular) Calcium - metabolism Calcium buffering Calcium efflux Calcium influx Calcium signalling Cardiac muscle Clonazepam - analogs & derivatives Clonazepam - pharmacology Computer Science Confocal Crosstalk Cytosol - drug effects Cytosol - metabolism Depolarization Efflux Electric Conductivity Firing rate Heart Heart diseases Heart Rate - drug effects Heart Ventricles - cytology Indoles - metabolism Inhibition Ion channels Kinases Laboratories Magnesium - pharmacology Medicine Mitochondria Mitochondria - drug effects Mitochondria - metabolism Models, Biological Myocytes, Cardiac - cytology Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Periodicity Permeability Predictive control Rabbits Rodents Ruthenium Compounds - pharmacology Ryanodine Receptor Calcium Release Channel - metabolism Sarcoplasmic reticulum Sarcoplasmic Reticulum - drug effects Sarcoplasmic Reticulum - metabolism Science Sinoatrial Node - cytology Sinoatrial Node - drug effects Sinoatrial Node - metabolism Sinoatrial Node - physiology Thiazepines - pharmacology Ventricle United States > US Maryland Baltimore Maryland
ISSN:	1932-6203, 1932-6203
Online-Zugang:	Volltext
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