ArticleJournal of molecular and cellular cardiology2011
Beat-to-beat Ca(2+)-dependent regulation of sinoatrial nodal pacemaker cell rate and rhythm.
Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 34 citations in OpenAlex.
- The mechano-electric feedback mediates the dual effect of stretch in mouse sinoatrial tissue.Journal of molecular and cellular cardiology plus · 2023Article
- What keeps us ticking? Sinoatrial node mechano-sensitivity: the grandfather clock of cardiac rhythm.Biophysical reviews · 2021Review
- Beating Rate Variability of Isolated Mammal Sinoatrial Node Tissue: Insight Into Its Contribution to Heart Rate Variability.Frontiers in neuroscience · 2020Article
- The Cardiac Pacemaker Story-Fundamental Role of the NaFrontiers in pharmacology · 2020Review
- Eliminating contraction during culture maintains global and local CaCell calcium · 2019Article
- Potential effects of intrinsic heart pacemaker cell mechanisms on dysrhythmic cardiac action potential firing.Frontiers in physiology · 2015Article
- From two competing oscillators to one coupled-clock pacemaker cell system.Frontiers in physiology · 2015Review
- The importance of Ca(2+)-dependent mechanisms for the initiation of the heartbeat.Frontiers in physiology · 2015Review
- Impaired signaling intrinsic to sinoatrial node pacemaker cells affects heart rate variability during cardiac disease.Journal of clinical trials · 2014Article
- Modern perspectives on numerical modeling of cardiac pacemaker cell.Journal of pharmacological sciences · 2014Review
- Mechanisms of beat-to-beat regulation of cardiac pacemaker cell function by Ca²⁺ cycling dynamics.Biophysical journal · 2013Article
- Age-related changes of myocardial ATP supply and demand mechanisms.Trends in endocrinology and metabolism: TEM · 2013Review
- Modern concepts concerning the origin of the heartbeat.Physiology (Bethesda, Md.) · 2013Review
- Article
- Optical imaging of voltage and calcium in cardiac cells & tissues.Circulation research · 2012Review
- The fractal-like complexity of heart rate variability beyond neurotransmitters and autonomic receptors: signaling intrinsic to sinoatrial node pacemaker cells.Cardiovascular pharmacology: open accessArticle
- Mechano-sensitivity of cardiac pacemaker function: pathophysiological relevance, experimental implications, and conceptual integration with other mechanisms of rhythmicity.Progress in biophysics and molecular biologyReview
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Whether intracellular Ca(2+) regulates sinoatrial node cell (SANC) action potential (AP) firing rate on a beat-to-beat basis is controversial. To directly test the hypothesis of beat-to-beat intracellular Ca(2+) regulation of the rate and rhythm of SANC we loaded single isolated SANC with a caged Ca(2+) buffer, NP-EGTA, and simultaneously recorded membrane potential and intracellular Ca(2+). Prior to introduction of the caged Ca(2+) buffer, spontaneous local Ca(2+) releases (LCRs) during diastolic depolarization were tightly coupled to rhythmic APs (r²=0.9). The buffer markedly prolonged the decay time (T₅₀) and moderately reduced the amplitude of the AP-induced Ca(2+) transient and partially depleted the SR load, suppressed spontaneous diastolic LCRs and uncoupled them from AP generation, and caused AP firing to become markedly slower and dysrhythmic. When Ca(2+) was acutely released from the caged compound by flash photolysis, intracellular Ca(2+) dynamics were acutely restored and rhythmic APs resumed immediately at a normal rate. After a few rhythmic cycles, however, these effects of the flash waned as interference with Ca(2+) dynamics by the caged buffer was reestablished. Our results directly support the hypothesis that intracellular Ca(2+) regulates normal SANC automaticity on a beat-to-beat basis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.