ArticleBiophysical journal2004
Diastolic calcium release controls the beating rate of rabbit sinoatrial node cells: numerical modeling of the coupling process.
Article in Biophysical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed.
- A new Fight-or-Flight Pacemaker Mechanism via Ryanodine Receptor abundance and superclustering.PLoS computational biology · 2026Article
- Dual effect of cardiac FKBP12.6 overexpression on excitation-contraction coupling and the incidence of ventricular arrhythmia depending on its expression level.Journal of molecular and cellular cardiology · 2024Article
- The evaluation of zebrafish cardiovascular and behavioral functions through microfluidics.Scientific reports · 2021Article
- Physiological Roles of the Rapidly Activated Delayed Rectifier KInternational journal of molecular sciences · 2021Article
- Pacing made easy: dynamic clamp promotes quantitative understanding of cardiac autorhythmicity and boosts the development of new pacemakers.Pflugers Archiv : European journal of physiology · 2020Article
- The Cardiac Pacemaker Story-Fundamental Role of the NaFrontiers in pharmacology · 2020Review
- Conservation of cardiac L-type CaJournal of molecular and cellular cardiology · 2018Article
- Different Profile of mRNA Expression in Sinoatrial Node from Streptozotocin-Induced Diabetic Rat.PloS one · 2016Article
- Nonlinear and Stochastic Dynamics in the Heart.Physics reports · 2014Article
- Hierarchical clustering of ryanodine receptors enables emergence of a calcium clock in sinoatrial node cells.The Journal of general physiology · 2014Article
- Modern perspectives on numerical modeling of cardiac pacemaker cell.Journal of pharmacological sciences · 2014Review
- Genetic isolation of stem cell-derived pacemaker-nodal cardiac myocytes.Molecular and cellular biochemistry · 2013Article
- Article
- A mathematical model of action potentials of mouse sinoatrial node cells with molecular bases.American journal of physiology. Heart and circulatory physiology · 2011Article
- Synchronization of stochastic Ca²(+) release units creates a rhythmic Ca²(+) clock in cardiac pacemaker cells.Biophysical journal · 2011Article
- Inhibition of spontaneous activity of rabbit atrioventricular node cells by KB-R7943 and inhibitors of sarcoplasmic reticulum Ca(2+) ATPase.Cell calcium · 2011Article
- Cardiac calmodulin kinase: a potential target for drug design.Current medicinal chemistry · 2011Review
- A coupled SYSTEM of intracellular Ca2+ clocks and surface membrane voltage clocks controls the timekeeping mechanism of the heart's pacemaker.Circulation research · 2010Review
- Yin and yang of the cardiac pacemaker clock system in health and disease.Heart rhythm · 2010Article
- Cholinergic receptor signaling modulates spontaneous firing of sinoatrial nodal cells via integrated effects on PKA-dependent Ca(2+) cycling and I(KACh).American journal of physiology. Heart and circulatory physiology · 2009Article
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Authors and funding
5 authors.
Funding
Abstract
Recent studies employing Ca2+ indicators and confocal microscopy demonstrate substantial local Ca2+ release beneath the cell plasma membrane (subspace) of sinoatrial node cells (SANCs) occurring during diastolic depolarization. Pharmacological and biophysical experiments have suggested that the released Ca2+ interacts with the plasma membrane via the ion current (INaCa) produced by the Na+/Ca2+ exchanger and constitutes an important determinant of the pacemaker rate. This study provides a numerical validation of the functional importance of diastolic Ca2+ release for rate control. The subspace Ca2+ signals in rabbit SANCs were measured by laser confocal microscopy, averaged, and calibrated. The time course of the subspace [Ca2+] displayed both diastolic and systolic components. The diastolic component was mainly due to the local Ca2+ releases; it was numerically approximated and incorporated into a SANC cellular electrophysiology model. The model predicts that the diastolic Ca2+ release strongly interacts with plasma membrane via INaCa and thus controls the phase of the action potential upstroke and ultimately the final action potential rate.
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