ArticleBiophysical journal2001
Dynamic regulation of sarcoplasmic reticulum Ca(2+) content and release by luminal Ca(2+)-sensitive leak in rat ventricular myocytes.
Article in Biophysical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed.
- Ryanodine receptor cluster remodeling linksbioRxiv : the preprint server for biology · 2026Article
- Structural and Functional Regulation of RyR2 in Cardiac Calcium Handling and Arrhythmogenesis.Biomedicines · 2026Review
- Sarcoplasmic reticulum-mitochondria microdomains: hugging and kissing in the heart.American journal of physiology. Cell physiology · 2025Review
- New N-aryl-N-alkyl-thiophene-2-carboxamide compound enhances intracellular CaBiophysical journal · 2023Article
- A Stochastic Spatiotemporal Model of Rat Ventricular Myocyte Calcium Dynamics Demonstrated Necessary Features for Calcium Wave Propagation.Membranes · 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
- Calcium signalling in mammalian cell lines expressing wild type and mutant human α1-Antitrypsin.Scientific reports · 2019Article
- The 4q25 variant rs13143308T links risk of atrial fibrillation to defective calcium homoeostasis.Cardiovascular research · 2019Article
- Toll-like receptor 4-induced ryanodine receptor 2 oxidation and sarcoplasmic reticulum CaThe Journal of biological chemistry · 2018Article
- Ambiguous interactions between diastolic and SR CaThe Journal of general physiology · 2017Review
- Calcium-induced calcium release supports recruitment of synaptic vesicles in auditory hair cells.Journal of neurophysiology · 2016Article
- Intracellular Na+ overload causes oxidation of CaMKII and leads to Ca2+ mishandling in isolated ventricular myocytes.Journal of molecular and cellular cardiology · 2014Article
- Cardiac ryanodine receptor activation by a high Ca²⁺ store load is reversed in a reducing cytoplasmic redox environment.Journal of cell science · 2014Article
- Life and death of a cardiac calcium spark.The Journal of general physiology · 2013Article
- 'Ryanopathy': causes and manifestations of RyR2 dysfunction in heart failure.Cardiovascular research · 2013Review
- Up-regulation of sarcoplasmic reticulum Ca(2+) uptake leads to cardiac hypertrophy, contractile dysfunction and early mortality in mice deficient in CASQ2.Cardiovascular research · 2013Article
- Dynamics of early afterdepolarization-mediated triggered activity in cardiac monolayers.Biophysical journal · 2012Article
- Calsequestrin 2 and arrhythmias.American journal of physiology. Heart and circulatory physiology · 2012Review
- Construction of calcium release sites in cardiac myocytes.Frontiers in physiology · 2012Article
- Dynamics of calcium sparks and calcium leak in the heart.Biophysical journal · 2011Article
11 more citing papers are in PubMed but not listed here.
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5 authors.
Funding
Abstract
In cardiac muscle, excitation-contraction (E-C) coupling is determined by the ability of the sarcoplasmic reticulum (SR) to store and release Ca(2+). It has been hypothesized that the Ca(2+) sequestration and release mechanisms might be functionally linked to optimize the E-C coupling process. To explore the relationships between the loading status of the SR and functional state of the Ca(2+) release mechanism, we examined the effects of changes in SR Ca(2+) content on spontaneous Ca(2+) sparks in saponin-permeabilized and patch-clamped rat ventricular myocytes. SR Ca(2+) content was manipulated by pharmacologically altering the capacities of either Ca(2+) uptake or leak. Ca(2+) sparks were recorded using a confocal microscope and Fluo-3 and were quantified considering missed events. SR Ca(2+) content was assessed by application of caffeine. Exposure of permeabilized cells to anti-phospholamban antibodies elevated the SR Ca(2+) content and increased the frequency of sparks. Suppression of the SR Ca(2+) pump by thapsigargin lowered [Ca(2+)](SR) and reduced the frequency of sparks. The ryanodine receptor (RyR) blockers tetracaine and Mg(2+) transiently suppressed the frequency of sparks. Upon washout of the drugs, sparking activity transiently overshot control levels. Low doses of caffeine transiently potentiated sparking activity upon application and transiently depressed the sparks upon removal. In patch-clamped cardiac myocytes, exposure to caffeine produced only a transient increase in the probability of sparks induced by depolarization. We interpret these results in terms of a novel dynamic control scheme for SR Ca(2+) cycling. A central element of this scheme is a luminal Ca(2+) sensor that links the functional activity of RyRs to the loading state of the SR, allowing cells to auto-regulate the size and functional state of their SR Ca(2+) pool. These results are important for understanding the regulation of intracellular Ca(2+) release and contractility in cardiac muscle.
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