ArticleBiophysical journal2008
Allosteric activation of Na+-Ca2+ exchange by L-type Ca2+ current augments the trigger flux for SR Ca2+ release in ventricular myocytes.
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 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- SERCA2 phosphorylation at serine 663 is a key regulator of CaNature communications · 2023Article
- A privileged role for neuronal NaThe Journal of general physiology · 2018Article
- Computational modeling of amylin-induced calcium dysregulation in rat ventricular cardiomyocytes.Cell calcium · 2018Article
- Neuronal sodium channels: emerging components of the nano-machinery of cardiac calcium cycling.The Journal of physiology · 2017Review
- Modeling NaJournal of molecular and cellular cardiology · 2016Article
- Na+/Ca2+ exchange and Na+/K+-ATPase in the heart.The Journal of physiology · 2015Review
- Na/Ca exchange and contraction of the heart.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
- Cardiac Na+-Ca2+ exchanger: dynamics of Ca2+-dependent activation and deactivation in intact myocytes.The Journal of physiology · 2013Article
- Na+/Ca2+ exchanger-1 protects against systolic failure in the Akitains2 model of diabetic cardiomyopathy via a CXCR4/NF-κB pathway.American journal of physiology. Heart and circulatory physiology · 2012Article
- Dynamic local changes in sarcoplasmic reticulum calcium: physiological and pathophysiological roles.Journal of molecular and cellular cardiology · 2012Review
- 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
- Cardiac myocytes and local signaling in nano-domains.Progress in biophysics and molecular biology · 2011Review
- Microdomain [Ca²⁺] near ryanodine receptors as reported by L-type Ca²⁺ and Na+/Ca²⁺ exchange currents.The Journal of physiology · 2011Article
- Subcellular heterogeneity of ryanodine receptor properties in ventricular myocytes with low T-tubule density.PloS one · 2011Article
- Na+ currents are required for efficient excitation-contraction coupling in rabbit ventricular myocytes: a possible contribution of neuronal Na+ channels.The Journal of physiology · 2010Article
- Activation of reverse Na+-Ca2+ exchange by the Na+ current augments the cardiac Ca2+ transient: evidence from NCX knockout mice.The Journal of physiology · 2010Article
- Organization of ryanodine receptors, transverse tubules, and sodium-calcium exchanger in rat myocytes.Biophysical journal · 2009Article
- Excitation-contraction coupling gain in ventricular myocytes: insights from a parsimonious model.The Journal of physiology · 2009Article
- Dysregulated sarcoplasmic reticulum calcium release: potential pharmacological target in cardiac disease.Pharmacology & therapeutics · 2008Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
The possible contribution of Na(+)-Ca(2+) exchange to the triggering of Ca(2+) release from the sarcoplasmic reticulum in ventricular cells remains unresolved. To gain insight into this issue, we measured the "trigger flux" of Ca(2+) crossing the cell membrane in rabbit ventricular myocytes with Ca(2+) release disabled pharmacologically. Under conditions that promote Ca(2+) entry via Na(+)-Ca(2+) exchange, internal [Na(+)] (10 mM), and positive membrane potential, the Ca(2+) trigger flux (measured using a fluorescent Ca(2+) indicator) was much greater than the Ca(2+) flux through the L-type Ca(2+) channel, indicating a significant contribution from Na(+)-Ca(2+) exchange to the trigger flux. The difference between total trigger flux and flux through L-type Ca(2+) channels was assessed by whole-cell patch-clamp recordings of Ca(2+) current and complementary experiments in which internal [Na(+)] was reduced. However, Ca(2+) entry via Na(+)-Ca(2+) exchange measured in the absence of L-type Ca(2+) current was considerably smaller than the amount inferred from the trigger flux measurements. From these results, we surmise that openings of L-type Ca(2+) channels increase [Ca(2+)] near Na(+)-Ca(2+) exchanger molecules and activate this protein. These results help to resolve seemingly contradictory results obtained previously and have implications for our understanding of the triggering of Ca(2+) release in heart cells under various conditions.
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Registered trials
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.