ArticleThe Journal of physiology2009
Intra-sarcoplasmic reticulum Ca2+ oscillations are driven by dynamic regulation of ryanodine receptor function by luminal Ca2+ in cardiomyocytes.
Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Structural and Functional Regulation of RyR2 in Cardiac Calcium Handling and Arrhythmogenesis.Biomedicines · 2026Review
- CaCells · 2024Review
- Physiology of intracellular calcium buffering.Physiological reviews · 2023Review
- NOS1AP polymorphisms reduce NOS1 activity and interact with prolonged repolarization in arrhythmogenesis.Cardiovascular research · 2021Article
- Buffering and total calcium levels determine the presence of oscillatory regimes in cardiac cells.PLoS computational biology · 2020Article
- Neuronal NaJACC. Basic to translational science · 2016Article
- Abnormal calcium cycling and cardiac arrhythmias associated with the human Ser96Ala genetic variant of histidine-rich calcium-binding protein.Journal of the American Heart Association · 2013Article
- Functional interaction between calsequestrin and ryanodine receptor in the heart.Cellular and molecular life sciences : CMLS · 2013Review
- Decoding myocardial Ca²⁺ signals across multiple spatial scales: a role for sensitivity analysis.Journal of molecular and cellular cardiology · 2013Review
- Store-dependent deactivation: cooling the chain-reaction of myocardial calcium signaling.Journal of molecular and cellular cardiology · 2013Review
- Posttranslational modifications of cardiac ryanodine receptors: Ca(2+) signaling and EC-coupling.Biochimica et biophysica acta · 2013Review
- Ca²⁺-dependent phosphorylation of Ca²⁺ cycling proteins generates robust rhythmic local Ca²⁺ releases in cardiac pacemaker cells.Science signaling · 2013Article
- Calsequestrin mutations and catecholaminergic polymorphic ventricular tachycardia.Pediatric cardiology · 2012Review
- Intercellular Ca(2+) waves: mechanisms and function.Physiological reviews · 2012Review
- Calsequestrin 2 and arrhythmias.American journal of physiology. Heart and circulatory physiology · 2012Review
- Shortened Ca2+ signaling refractoriness underlies cellular arrhythmogenesis in a postinfarction model of sudden cardiac death.Circulation research · 2012Article
- Dynamic local changes in sarcoplasmic reticulum calcium: physiological and pathophysiological roles.Journal of molecular and cellular cardiology · 2012Review
- Calsequestrin 2 deletion shortens the refractoriness of Ca²⁺ release and reduces rate-dependent Ca²⁺-alternans in intact mouse hearts.Journal of molecular and cellular cardiology · 2012Article
- Does the Goldilocks Principle apply to calcium release restitution in heart cells?Journal of molecular and cellular cardiology · 2012Article
- Toward an integrative computational model of the Guinea pig cardiac myocyte.Frontiers in physiology · 2012Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
During the cardiac cycle, the release of Ca(2+) from the sarcoplasmic reticulum (SR) through the ryanodine receptor (RyR2) channel complex is controlled by the levels of cytosolic and luminal Ca(2+) and alterations in these regulatory processes have been implicated in cardiac disease including arrhythmia. To better understand the mechanisms of regulation of SR Ca(2+) release by Ca(2+) on both sides of the SR membrane, we investigated SR Ca(2+) release in a wide range of cytosolic Ca(2+) concentrations ([Ca(2+)](cyt); 1-100 microm) in permeabilized canine ventricular myocytes by monitoring [Ca(2+)] inside the SR ([Ca(2+)](SR)). Exposing myocytes to activating [Ca(2+)](cyt) resulted in spontaneous oscillations of [Ca(2+)](SR) due to periodic opening and closing of the RyR2s. Elevating [Ca(2+)](cyt) (up to 10 microm) increased the frequency of [Ca(2+)](SR) oscillations; however at higher [Ca(2+)](cyt) (>50 microm) the oscillations diminished due to RyR2s staying perpetually open, resulting in depleted SR. Ablation of cardiac calsequestrin (CASQ2) altered the [Ca(2+)](cyt) dependence of Ca(2+) release oscillations such that oscillations were highly frequent at low [Ca(2+)](cyt) (100 nm) but became diminished at moderate [Ca(2+)](cyt) (10 microm), as determined in myocytes from calsequestrin-null versus wild-type mice. Our results suggest that under conditions of continuous activation by cytosolic Ca(2+), RyR2s can periodically cycle between open and deactivated states due to effects of luminal Ca(2+). Deactivation at reduced [Ca(2+)]SR appears to involve reduction of sensitivity to cytosolic Ca(2+) and might be mediated by CASQ2. Inactivation by cytosolic Ca(2+) plays no detectable role in controlling SR Ca(2+) release.
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