ArticleBiophysical journal2008
Ca2+-mobility in the sarcoplasmic reticulum of ventricular myocytes is low.
Article in Biophysical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 53 citations in OpenAlex.
- Modeling sarcoplasmic reticulum CaBiophysics reports · 2024Article
- Physiology of intracellular calcium buffering.Physiological reviews · 2023Review
- Image-Driven Modeling of Nanoscopic Cardiac Function: Where Have We Come From, and Where Are We Going?Frontiers in physiology · 2022Review
- A Stochastic Spatiotemporal Model of Rat Ventricular Myocyte Calcium Dynamics Demonstrated Necessary Features for Calcium Wave Propagation.Membranes · 2021Article
- Three-Dimensional Model of Sub-Plasmalemmal CaFrontiers in immunology · 2021Article
- Overview of the Microenvironment of Vasculature in Vascular Tone Regulation.International journal of molecular sciences · 2018Review
- Modulation of Cardiac Alternans by Altered Sarcoplasmic Reticulum Calcium Release: A Simulation Study.Frontiers in physiology · 2018Article
- The intricacies of atrial calcium cycling during excitation-contraction coupling.The Journal of general physiology · 2017Review
- Regional acidosis locally inhibits but remotely stimulates Ca2+ waves in ventricular myocytes.Cardiovascular research · 2017Article
- Visualization of Ca2+ Filling Mechanisms upon Synaptic Inputs in the Endoplasmic Reticulum of Cerebellar Purkinje Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Ca2+ Diffusion through Endoplasmic Reticulum Supports Elevated Intraterminal Ca2+ Levels Needed to Sustain Synaptic Release from Rods in Darkness.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- A human ventricular myocyte model with a refined representation of excitation-contraction coupling.Biophysical journal · 2015Article
- Na⁺ ions as spatial intracellular messengers for co-ordinating Ca²⁺ signals during pH heterogeneity in cardiomyocytes.Cardiovascular research · 2015Article
- Oxidative stress and ca(2+) release events in mouse cardiomyocytes.Biophysical journal · 2014Article
- Spatially defined InsP3-mediated signaling in embryonic stem cell-derived cardiomyocytes.PloS one · 2014Article
- Ca²⁺ waves in the heart.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
- Calcium movements inside the sarcoplasmic reticulum of cardiac myocytes.Journal of molecular and cellular cardiology · 2013Review
- Alterations in T-tubule and dyad structure in heart disease: challenges and opportunities for computational analyses.Cardiovascular research · 2013Review
- Extraction of sub-microscopic Ca fluxes from blurred and noisy fluorescent indicator images with a detailed model fitting approach.PLoS computational biology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
The sarcoplasmic reticulum (SR) in ventricular myocytes contains releasable Ca(2+) for activating cellular contraction. Recent measurements of intra-SR (luminal) Ca(2+) suggest a high diffusive Ca(2+)-mobility constant (D(CaSR)). This could help spatially to unify SR Ca(2+)-content ([Ca(2+)](SRT)) and standardize Ca(2+)-release throughout the cell. But measurements of localized depletions of luminal Ca(2+) (Ca(2+)-blinks), associated with local Ca(2+)-release (Ca(2+)-sparks), suggest D(CaSR) may actually be low. Here we describe a novel method for measuring D(CaSR). Using a cytoplasmic Ca(2+)-fluorophore, we estimate regional [Ca(2+)](SRT) from localized, caffeine-induced SR Ca(2+)-release. Caffeine microperfusion of one end of a guinea pig or rat myocyte diffusively empties the whole SR at a rate indicating D(CaSR) is 8-9 microm(2)/s, up to tenfold lower than previous estimates. Ignoring background SR Ca(2+)-leakage in our measurement protocol produces an artifactually high D(CaSR) (>40 microm(2)/s), which may also explain the previous high values. Diffusion-reaction modeling suggests that a low D(CaSR) would be sufficient to support local SR Ca(2+)-signaling within sarcomeres during excitation-contraction coupling. Low D(CaSR) also implies that [Ca(2+)](SRT) may readily become spatially nonuniform, particularly under pathological conditions of spatially nonuniform Ca(2+)-release. Local control of luminal Ca(2+), imposed by low D(CaSR), may complement the well-established local control of SR Ca(2+)-release by Ca(2+)-channel/ryanodine receptor couplons.
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Registered trials
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