ArticlePloS one2012
Crosstalk between mitochondrial and sarcoplasmic reticulum Ca2+ cycling modulates cardiac pacemaker cell automaticity.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- Intracellular CaInternational journal of molecular sciences · 2026Article
- Lysosomal CaPNAS nexus · 2023Article
- Physiological and Pathophysiological Roles of Mitochondrial NaBiomolecules · 2021Review
- May the Force Not Be With You During Culture: Eliminating Mechano-Associated Feedback During Culture Preserves Cultured Atrial and Pacemaker Cell Functions.Frontiers in physiology · 2020Review
- A Spatiotemporal Ventricular Myocyte Model Incorporating Mitochondrial Calcium Cycling.Biophysical journal · 2019Article
- SR-mitochondria communication in adult cardiomyocytes: A close relationship where the CaArchives of biochemistry and biophysics · 2019Review
- Scaling and correlation properties of RR and QT intervals at the cellular level.Scientific reports · 2019Article
- Mitochondrial CaPharmacology & therapeutics · 2018Review
- Bioenergetic Feedback between Heart Cell Contractile Machinery and Mitochondrial 3D Deformations.Biophysical journal · 2018Article
- Unique CaInternational journal of molecular sciences · 2018Review
- Mitochondrial Ca2+ flux modulates spontaneous electrical activity in ventricular cardiomyocytes.PloS one · 2018Article
- Involvement of mitochondrial permeability transition pore (mPTP) in cardiac arrhythmias: Evidence from cyclophilin D knockout mice.Cell calcium · 2016Article
- Electrochemical Na+ and Ca2+ gradients drive coupled-clock regulation of automaticity of isolated rabbit sinoatrial nodal pacemaker cells.American journal of physiology. Heart and circulatory physiology · 2016Article
- Regionally diverse mitochondrial calcium signaling regulates spontaneous pacing in developing cardiomyocytes.Cell calcium · 2015Article
- The destiny of Ca(2+) released by mitochondria.The journal of physiological sciences : JPS · 2015Review
- Spatiotemporal stability of neonatal rat cardiomyocyte monolayers spontaneous activity is dependent on the culture substrate.PloS one · 2015Article
- From beat rate variability in induced pluripotent stem cell-derived pacemaker cells to heart rate variability in human subjects.Heart rhythm · 2014Article
- Cardiac responses to β-adrenoceptor stimulation is partly dependent on mitochondrial calcium uniporter activity.British journal of pharmacology · 2014Article
- Modern perspectives on numerical modeling of cardiac pacemaker cell.Journal of pharmacological sciences · 2014Review
- Numerical Modeling Calcium and CaMKII Effects in the SA Node.Frontiers in pharmacology · 2014Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
backgroundMitochondria 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).
objectiveTo 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.
resultsInhibition 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).
conclusionA 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.
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