ArticleThe Journal of general physiology1999
Rapid activation of the cardiac ryanodine receptor by submillisecond calcium stimuli.
Article in The Journal of general physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers, 1 of them a synthesis that pooled it.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Calcium and arrhythmogenesis.Physiological reviews · 2007Pooled it
- The role of subunit cooperativity on ryanodine receptor 2 calcium signaling.Biophysical journal · 2023Article
- Multi-Scale Computational Modeling of Spatial Calcium Handling From Nanodomain to Whole-Heart: Overview and Perspectives.Frontiers in physiology · 2022Review
- Myocardial and Arrhythmic Spectrum of Neuromuscular Disorders in Children.Biomolecules · 2021Review
- Mechanistic link between CaM-RyR2 interactions and the genesis of cardiac arrhythmia.Biophysical journal · 2021Article
- Magnesium Ions Moderate Calcium-Induced Calcium Release in Cardiac Calcium Release Sites by Binding to Ryanodine Receptor Activation and Inhibition Sites.Frontiers in physiology · 2021Article
- Structure and Function of the Human Ryanodine Receptors and Their Association with Myopathies-Present State, Challenges, and Perspectives.Molecules (Basel, Switzerland) · 2020Review
- Ryanodine Receptor 1-Related Myopathies: Diagnostic and Therapeutic Approaches.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- Quenching the spark: Termination of CICR in the submicroscopic space of the dyad.The Journal of general physiology · 2017Review
- Structures of the colossal RyR1 calcium release channel.Current opinion in structural biology · 2016Review
- Calcium spike variability in cardiac myocytes results from activation of small cohorts of ryanodine receptor 2 channels.The Journal of physiology · 2012Article
- Construction of calcium release sites in cardiac myocytes.Frontiers in physiology · 2012Article
- Quarky calcium release in the heart.Circulation research · 2011Article
- Frequency and release flux of calcium sparks in rat cardiac myocytes: a relation to RYR gating.The Journal of general physiology · 2010Article
- cAMP/PKA-dependent increases in Ca Sparks, oscillations and SR Ca stores in retinal arteriolar myocytes after exposure to vasopressin.Investigative ophthalmology & visual science · 2010Article
- Local calcium release activation by DHPR calcium channel openings in rat cardiac myocytes.The Journal of physiology · 2008Article
- Alternans of cardiac calcium cycling in a cluster of ryanodine receptors: a simulation study.American journal of physiology. Heart and circulatory physiology · 2008Article
- Protein geometry and placement in the cardiac dyad influence macroscopic properties of calcium-induced calcium release.Biophysical journal · 2007Article
- Kinetics of calcium spikes in rat cardiac myocytes.The Journal of physiology · 2007Article
- Mechanisms of excitation-contraction coupling in an integrative model of the cardiac ventricular myocyte.Biophysical journal · 2006Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
Abstract
The local control concept of excitation-contraction coupling in the heart postulates that the activity of the sarcoplasmic reticulum ryanodine receptor channels (RyR) is controlled by Ca(2+) entry through adjoining sarcolemmal single dihydropyridine receptor channels (DHPRs). One unverified premise of this hypothesis is that the RyR must be fast enough to track the brief (<0.5 ms) Ca(2+) elevations accompanying single DHPR channel openings. To define the kinetic limits of effective trigger Ca(2+) signals, we recorded activity of single cardiac RyRs in lipid bilayers during rapid and transient increases in Ca(2+) generated by flash photolysis of DM-nitrophen. Application of such Ca(2+) spikes (amplitude approximately 10-30 microM, duration approximately 0.1-0.4 ms) resulted in activation of the RyRs with a probability that increased steeply (apparent Hill slope approximately 2.5) with spike amplitude. The time constants of RyR activation were 0.07-0.27 ms, decreasing with spike amplitude. To fit the rising portion of the open probability, a single exponential function had to be raised to a power n approximately 3. We show that these data could be adequately described with a gating scheme incorporating four sequential Ca(2+)-sensitive closed states between the resting and the first open states. These results provide evidence that brief Ca(2+) triggers are adequate to activate the RyR, and support the possibility that RyR channels are governed by single DHPR openings. They also provide evidence for the assumption that RyR activation requires binding of multiple Ca(2+) ions in accordance with the tetrameric organization of the channel protein.
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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.