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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Vydáno v:	PloS one Ročník 7; číslo 5; s. e37582
Hlavní autoři:	Yaniv, Yael, Spurgeon, Harold A., Lyashkov, Alexey E., Yang, Dongmei, Ziman, Bruce D., Maltsev, Victor A., Lakatta, Edward G.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Public Library of Science 29.05.2012 Public Library of Science (PLoS)
Témata:	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
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Popis
Shrnutí:	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 SANC automaticity: LCRs activate an inward Na(+)-Ca(2+) exchange current to accelerate the diastolic depolarization, prompting the ensemble of surface membrane ion channels to generate the next action potential (AP). To determine if mitochondrial Ca(2+) (Ca(2+) (m)), cytosolic Ca(2+) (Ca(2+) (c))-SR-Ca(2+) crosstalk occurs in single rabbit SANC, and how this may relate to SANC normal automaticity. Inhibition of mitochondrial Ca(2+) influx into (Ru360) or Ca(2+) efflux from (CGP-37157) decreased [Ca(2+)](m) to 80 ± 8% control or increased [Ca(2+)](m) to 119 ± 7% control, respectively. Concurrent with inhibition of mitochondrial Ca(2+) influx or efflux, the SR Ca(2+) load, and LCR size, duration, amplitude and period (imaged via confocal linescan) significantly increased or decreased, respectively. Changes in total ensemble LCR Ca(2+) signal were highly correlated with the change in the SR Ca(2+) load (r(2) = 0.97). Changes in the spontaneous AP cycle length (Ru360, 111 ± 1% control; CGP-37157, 89 ± 2% control) in response to changes in [Ca(2+)](m) were predicted by concurrent changes in LCR period (r(2) = 0.84). A change in SANC Ca(2+) (m) flux translates into a change in the AP firing rate by effecting changes in Ca(2+) (c) and SR Ca(2+) loading, which affects the characteristics of spontaneous SR Ca(2+) release.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conceived and designed the experiments: EGL YY. Performed the experiments: YY AEL DY. Analyzed the data: YY AEL. Contributed reagents/materials/analysis tools: HAS BDZ VAM. Wrote the paper: EGL YY.
ISSN:	1932-6203 1932-6203
DOI:	10.1371/journal.pone.0037582