ArticleThe Journal of physiology2005
Paradoxical SR Ca2+ release in guinea-pig cardiac myocytes after beta-adrenergic stimulation revealed by two-photon photolysis of caged Ca2+.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- Abnormal phosphorylation / dephosphorylation and CaHeart failure reviews · 2024Review
- Local recovery of cardiac calcium-induced calcium release interrogated by ultra-effective, two-photon uncaging of calcium.The Journal of physiology · 2021Article
- Multiple targets for flecainide action: implications for cardiac arrhythmogenesis.British journal of pharmacology · 2018Review
- T-Tubular Electrical Defects Contribute to Blunted β-Adrenergic Response in Heart Failure.International journal of molecular sciences · 2016Article
- Calcium Uncaging with Visible Light.Journal of the American Chemical Society · 2016Article
- Posttranslational modifications of cardiac ryanodine receptors: Ca(2+) signaling and EC-coupling.Biochimica et biophysica acta · 2013Review
- Isoproterenol increases the fraction of spark-dependent RyR-mediated leak in ventricular myocytes.Biophysical journal · 2013Article
- Transcription factor CHF1/Hey2 regulates EC coupling and heart failure in mice through regulation of FKBP12.6.American journal of physiology. Heart and circulatory physiology · 2012Article
- Synthetic localized calcium transients directly probe signalling mechanisms in skeletal muscle.The Journal of physiology · 2012Article
- Role of chronic ryanodine receptor phosphorylation in heart failure and β-adrenergic receptor blockade in mice.The Journal of clinical investigation · 2010Article
- Phosphorylation of the ryanodine receptor mediates the cardiac fight or flight response in mice.The Journal of clinical investigation · 2010Article
- Acute heart failure with low cardiac output: can we develop a short-term inotropic agent that does not increase adverse events?Current heart failure reports · 2010Article
- Ryanodine receptor studies using genetically engineered mice.FEBS letters · 2010Review
- Increased Ca(2+) leak and spatiotemporal coherence of Ca(2+) release in cardiomyocytes during beta-adrenergic stimulation.The Journal of physiology · 2010Article
- Abnormalities of calcium metabolism and myocardial contractility depression in the failing heart.Heart failure reviews · 2009Review
- Redox modification of ryanodine receptors underlies calcium alternans in a canine model of sudden cardiac death.Cardiovascular research · 2009Article
- Beta-adrenergic signaling accelerates and synchronizes cardiac ryanodine receptor response to a single L-type Ca2+ channel.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Diastolic transient inward current in long QT syndrome type 3 is caused by Ca2+ overload and inhibited by ranolazine.Journal of molecular and cellular cardiology · 2009Article
- Ca2+/calmodulin kinase II increases ryanodine binding and Ca2+-induced sarcoplasmic reticulum Ca2+ release kinetics during beta-adrenergic stimulation.Journal of molecular and cellular cardiology · 2007Article
- Verrucotoxin, a stonefish venom, modulates calcium channel activity in guinea-pig ventricular myocytes.British journal of pharmacology · 2007Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In heart muscle the amplification and shaping of Ca(2+) signals governing contraction are orchestrated by recruiting a variable number of Ca(2+) sparks. Sparks reflect Ca(2+) release from the sarcoplasmic reticulum (SR) via Ca(2+) release channels (ryanodine receptors, RyRs). RyRs are activated by Ca(2+) influx via L-type Ca(2+) channels with a specific probability that may depend on regulatory mechanisms (e.g. beta-adrenergic stimulation) or diseased states (e.g. heart failure). Changes of RyR phosphorylation may be critical for both regulation and impaired function in disease. Using UV flash photolysis of caged Ca(2+) and short applications of caffeine in guinea-pig ventricular myocytes, we found that Ca(2+) release signals on the cellular level were largely governed by global SR content. During beta-adrenergic stimulation resting myocytes exhibited smaller SR Ca(2+) release signals when activated by photolysis (62.3% of control), resulting from reduced SR Ca(2+) content under these conditions (58.6% of control). In contrast, local signals triggered with diffraction limited two-photon photolysis displayed the opposite behaviour, exhibiting a larger Ca(2+) release (164% of control) despite reduced global and local SR Ca(2+) content. This apparent paradox implies changes of RyR open probabilities after beta-adrenergic stimulation, enhancing local regenerativity and reliability of Ca(2+) signalling. Thus, our results underscore the importance of phosphorylation of RyRs (or of a related protein), as a regulatory physiological mechanism that may also provide new therapeutic avenues to recover impaired Ca(2+) signalling during cardiac disease.
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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.