ArticleThe Journal of physiology2008
Local calcium release activation by DHPR calcium channel openings in rat cardiac myocytes.
Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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26 citing papers in PubMed, 41 citations in OpenAlex.
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- Mechanisms and physiological implications of cooperative gating of clustered ion channels.Physiological reviews · 2022Review
- Structure and Function of the Human Ryanodine Receptors and Their Association with Myopathies-Present State, Challenges, and Perspectives.Molecules (Basel, Switzerland) · 2020Review
- Structural variability of dyads relates to calcium release in rat ventricular myocytes.Scientific reports · 2020Article
- Long-term high-altitude hypoxia influences pulmonary arterial L-type calcium channel-mediated CaAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2018Article
- Sub-cellular Electrical Heterogeneity Revealed by Loose Patch Recording Reflects Differential Localization of Sarcolemmal Ion Channels in Intact Rat Hearts.Frontiers in physiology · 2018Article
- Ryanodine receptor gating controls generation of diastolic calcium waves in cardiac myocytes.The Journal of general physiology · 2015Article
- A modified local control model for Ca2+ transients in cardiomyocytes: junctional flux is accompanied by release from adjacent non-junctional RyRs.Journal of molecular and cellular cardiology · 2014Article
- Ca2+ channel nanodomains boost local Ca2+ amplitude.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Article
- Cardiac sodium-calcium exchange and efficient excitation-contraction coupling: implications for heart disease.Advances in experimental medicine and biology · 2013Review
- Calcium spike variability in cardiac myocytes results from activation of small cohorts of ryanodine receptor 2 channels.The Journal of physiology · 2012Article
- Modeling effects of L-type ca(2+) current and na(+)-ca(2+) exchanger on ca(2+) trigger flux in rabbit myocytes with realistic T-tubule geometries.Frontiers in physiology · 2012Article
- How does the ryanodine receptor in the ventricular myocyte wake up: by a single or by multiple open L-type Ca2+ channels?European biophysics journal : EBJ · 2012Article
- The interaction of Ca2+ with sarcomeric proteins: role in function and dysfunction of the heart.American journal of physiology. Heart and circulatory physiology · 2012Review
- Dynamics of calcium sparks and calcium leak in the heart.Biophysical journal · 2011Article
- Electromechanical coupling in the cardiac myocyte; stretch-arrhythmia feedback.Pflugers Archiv : European journal of physiology · 2011Review
- Analysis of Cav1.2 and ryanodine receptor clusters in rat ventricular myocytes.Biophysical journal · 2010Article
- How does the shape of the cardiac action potential control calcium signaling and contraction in the heart?Journal of molecular and cellular cardiology · 2010Article
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5 authors at 1 institution in 1 country.
Funding
Abstract
The principal role of calcium current in the triggering of calcium release in cardiac myocytes is well recognized. The mechanism of how calcium current (I(Ca)) controls the intensity of calcium release is not clear because of the stochastic nature of voltage-dependent gating of calcium channels (DHPRs) and of calcium-dependent gating of ryanodine receptors (RyRs). To disclose the relation between DHPR openings and the probability of calcium release, local calcium release activation by I(Ca) was investigated in rat ventricular myocytes using patch-clamp and confocal microscopy. Calcium spikes were activated by temporally synchronized DHPR calcium current triggers, generated by instantaneous 'tail' I(Ca) and modulated by prepulse duration, by tail potential, and by the DHPR agonist BayK 8644. The DHPR-RyR coupling fidelity was determined from the temporal distribution of calcium spike latencies using a model based on exponentially distributed DHPR open times. The analysis provided a DHPR mean open time of approximately 0.5 ms, RyR activation time constant of approximately 0.6 ms, and RyR activation kinetics of the 4th order. The coupling fidelity was low due to the inherent prevalence of very short DHPR openings but was increased when DHPR openings were prolonged by BayK 8644. The probability of calcium release activation was high, despite low coupling fidelity, due to the activation of many DHPRs at individual release sites. We conclude that the control of calcium release intensity by physiological stimuli can be achieved by modulating the number and duration of DHPR openings at low coupling fidelity, thus avoiding the danger of inadvertently triggering calcium release events.
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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.