ArticleThe Journal of physiology2009
Alteration of sarcoplasmic reticulum Ca2+ release termination by ryanodine receptor sensitization and in heart failure.
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 58 papers.
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Who cites it
58 citing papers in PubMed, 69 citations in OpenAlex.
- The endoplasmic reticulum luminal CaPNAS nexus · 2025Article
- Using a Failing Human Ventricular Cardiomyocyte Model to Re-Evaluate CaBiomolecules · 2024Article
- Study of amphipathic metabolites in cardiac pathophysiology: Insights gained from long-chain acylcarnitines and calcium handling.Journal of cellular and molecular medicine · 2023Article
- Cysteines 1078 and 2991 cross-linking plays a critical role in redox regulation of cardiac ryanodine receptor (RyR).Nature communications · 2023Article
- Melatonin to Rescue the Aged Heart: Antiarrhythmic and Antioxidant Benefits.Oxidative medicine and cellular longevity · 2021Review
- Calcium-induced calcium release in astroglia-a view "from the inside".Pflugers Archiv : European journal of physiology · 2020Article
- Oxidation of ryanodine receptor after ischemia-reperfusion increases propensity of CaAmerican journal of physiology. Heart and circulatory physiology · 2018Article
- The role of RyR2 oxidation in the blunted frequency-dependent facilitation of CaPflugers Archiv : European journal of physiology · 2018Article
- FK506-binding proteins 12 and 12.6 (FKBPs) as regulators of cardiac Ryanodine Receptors: Insights from new functional and structural knowledge.Channels (Austin, Tex.) · 2017Review
- Dysregulated ZnThe Journal of biological chemistry · 2017Article
- The effect of PKA-mediated phosphorylation of ryanodine receptor on SR CaJournal of molecular and cellular cardiology · 2017Article
- Dyssynchronous calcium removal in heart failure-induced atrial remodeling.American journal of physiology. Heart and circulatory physiology · 2016Article
- L30A Mutation of Phospholemman Mimics Effects of Cardiac Glycosides in Isolated Cardiomyocytes.Biochemistry · 2016Article
- Cardiac Calcium ATPase Dimerization Measured by Cross-Linking and Fluorescence Energy Transfer.Biophysical journal · 2016Article
- R-CEPIA1er as a new tool to directly measure sarcoplasmic reticulum [Ca] in ventricular myocytes.American journal of physiology. Heart and circulatory physiology · 2016Article
- Increased Energy Demand during Adrenergic Receptor Stimulation Contributes to Ca(2+) Wave Generation.Biophysical journal · 2015Article
- Cytosolic Ca²⁺ buffering determines the intra-SR Ca²⁺ concentration at which cardiac Ca²⁺ sparks terminate.Cell calcium · 2015Article
- Inositol-1,4,5-trisphosphate induced Ca2+ release and excitation-contraction coupling in atrial myocytes from normal and failing hearts.The Journal of physiology · 2015Article
- Decreased inward rectifying K+ current and increased ryanodine receptor sensitivity synergistically contribute to sustained focal arrhythmia in the intact rabbit heart.The Journal of physiology · 2015Article
- Acute inotropic and lusitropic effects of cardiomyopathic R9C mutation of phospholamban.The Journal of biological chemistry · 2015Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
Many physiological processes and pharmacological agents modulate the ryanodine receptor (RyR), the primary sarcoplasmic reticulum (SR) Ca(2+) release channel in the heart. However, how such modulations translate into functional effects during cardiac excitation-contraction coupling (ECC) is much less clear. Using a low dose (250 microM) of caffeine we sensitized the RyR and examined SR Ca(2+) release using dynamic measurements of cytosolic Ca(2+) ([Ca(2+)](i)) and free Ca(2+) within the SR ([Ca(2+)](SR)). In field stimulated (1 Hz) rabbit ventricular myocytes, application of 250 microM caffeine caused an initial 33% increase in SR Ca(2+) release, which was followed by a decrease in SR Ca(2+) load (28%) and steady-state SR Ca(2+) release (23%). To investigate the effects of caffeine on local SR Ca(2+) release, we measured [Ca(2+)](SR) from individual release junctions during ECC as well as during spontaneous Ca(2+) sparks. In intact myocytes during ECC, caffeine increased global fractional SR Ca(2+) release by decreasing the [Ca(2+)](SR) level at which local release terminated by 21%. Similarly, in permeabilized myocytes during spontaneous Ca(2+) sparks, caffeine decreased the [Ca(2+)](SR) level for release termination by 12%. Finally, we examined if Ca(2+) release termination was changed in myocytes from failing hearts, where remodelling processes lead to altered RyR function. In myocytes from failing rabbit hearts, the [Ca(2+)](SR) termination level for Ca(2+) sparks was 13% lower than that of non-failing myocytes. Collectively, these data suggest that altering the termination level for local Ca(2+) release may represent a novel mechanism to increase SR Ca(2+) release and contractility during ECC.
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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.