ArticleBiophysical journal2013
Mechanisms of beat-to-beat regulation of cardiac pacemaker cell function by Ca²⁺ cycling dynamics.
Article in Biophysical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Developing cardiac biomechanical models beyond the clinic: modeling stressors of daily life.Biomechanics and modeling in mechanobiology · 2025Review
- A novel perspective on the regulation of cardiac cell beating: cardiac cell under mechanical stimulation acts as "cell activation button" to activate adjacent cardiac cell.Journal of nanobiotechnology · 2025Article
- The electrophysiological effects of Tongyang Huoxue granules on the ignition phase during hypoxia/reoxygenation injury in sinoatrial node cells.Frontiers in physiology · 2024Article
- The mechano-electric feedback mediates the dual effect of stretch in mouse sinoatrial tissue.Journal of molecular and cellular cardiology plus · 2023Article
- Diversity of cells and signals in the cardiovascular system.The Journal of physiology · 2023Article
- Indirect evidence that anoxia exposure and cold acclimation alter transarcolemmal CaComparative biochemistry and physiology. Part A, Molecular & integrative physiology · 2021Article
- Self-Similar Synchronization of Calcium and Membrane Potential Transitions During Action Potential Cycles Predict Heart Rate Across Species.JACC. Clinical electrophysiology · 2021Article
- Article
- Respiratory regulation & interactions with neuro-cognitive circuitry.Neuroscience and biobehavioral reviews · 2020Review
- The Cardiac Pacemaker Story-Fundamental Role of the NaFrontiers in pharmacology · 2020Review
- Calcium Buffering in the Heart in Health and Disease.Circulation · 2019Review
- Eliminating contraction during culture maintains global and local CaCell calcium · 2019Article
- Novel NaFrontiers in pharmacology · 2019Article
- Heterogeneity of calcium clock functions in dormant, dysrhythmically and rhythmically firing single pacemaker cells isolated from SA node.Cell calcium · 2018Article
- Spontaneous, local diastolic subsarcolemmal calcium releases in single, isolated guinea-pig sinoatrial nodal cells.PloS one · 2017Article
- 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
- Current understanding of the pathophysiological mechanisms responsible for inappropriate sinus tachycardia: role of the If "funny" current.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2016Review
- The Autonomic Nervous System Regulates the Heart Rate through cAMP-PKA Dependent and Independent Coupled-Clock Pacemaker Cell Mechanisms.Frontiers in physiology · 2016Article
- Arrhythmogenesis in a catecholaminergic polymorphic ventricular tachycardia mutation that depresses ryanodine receptor function.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Spatiotemporal stability of neonatal rat cardiomyocyte monolayers spontaneous activity is dependent on the culture substrate.PloS one · 2015Article
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Authors and funding
4 authors.
Funding
Abstract
Whether intracellular Ca(2+) cycling dynamics regulate cardiac pacemaker cell function on a beat-to-beat basis remains unknown. Here we show that under physiological conditions, application of low concentrations of caffeine (2-4 mM) to isolated single rabbit sinoatrial node cells acutely reduces their spontaneous action potential cycle length (CL) and increases Ca(2+) transient amplitude for several cycles. Numerical simulations, using a modified Maltsev-Lakatta coupled-clock model, faithfully reproduced these effects, and also the effects of CL prolongation and dysrhythmic spontaneous beating (produced by cytosolic Ca(2+) buffering) and an acute CL reduction (produced by flash-induced Ca(2+) release from a caged Ca(2+) buffer), which we had reported previously. Three contemporary numerical models (including the original Maltsev-Lakatta model) failed to reproduce the experimental results. In our proposed new model, Ca(2+) releases acutely change the CL via activation of the Na(+)/Ca(2+) exchanger current. Time-dependent CL reductions after flash-induced Ca(2+) releases (the memory effect) are linked to changes in Ca(2+) available for pumping into sarcoplasmic reticulum which, in turn, changes the sarcoplasmic reticulum Ca(2+) load, diastolic Ca(2+) releases, and Na(+)/Ca(2+) exchanger current. These results support the idea that Ca(2+) regulates CL in cardiac pacemaker cells on a beat-to-beat basis, and suggest a more realistic numerical mechanism of this regulation.
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