ArticleThe Journal of physiology2004
Control of intracellular calcium in the presence of nitric oxide donors in isolated skeletal muscle fibres from mouse.
Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Probenecid affects muscle Ca2+ homeostasis and contraction independently from pannexin channel block.The Journal of general physiology · 2023Article
- Pannexin-1 and CaV1.1 show reciprocal interaction during excitation-contraction and excitation-transcription coupling in skeletal muscle.The Journal of general physiology · 2021Article
- Preserved CaDiabetologia · 2020Article
- Dietary Nitrate Enhances the Contractile Properties of Human Skeletal Muscle.Exercise and sport sciences reviews · 2018Review
- Mechanisms Explaining Muscle Fatigue and Muscle Pain in Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): a Review of Recent Findings.Current rheumatology reports · 2017Review
- The Neuro-Immune Pathophysiology of Central and Peripheral Fatigue in Systemic Immune-Inflammatory and Neuro-Immune Diseases.Molecular neurobiology · 2016Review
- Improved tolerance of acute severe hypoxic stress in chronic hypoxic diaphragm is nitric oxide-dependent.The journal of physiological sciences : JPS · 2015Article
- Genetically enhancing mitochondrial antioxidant activity improves muscle function in aging.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Confocal imaging of transmembrane voltage by SEER of di-8-ANEPPS.The Journal of general physiology · 2013Article
- Acute effects of reactive oxygen and nitrogen species on the contractile function of skeletal muscle.The Journal of physiology · 2011Review
- Modulation of contractile apparatus Ca2+ sensitivity and disruption of excitation-contraction coupling by S-nitrosoglutathione in rat muscle fibres.The Journal of physiology · 2011Article
- Altered myoplasmic Ca(2+) handling in rat fast-twitch skeletal muscle fibres during disuse atrophy.Pflugers Archiv : European journal of physiology · 2010Article
- Expression of the muscular dystrophy-associated caveolin-3(P104L) mutant in adult mouse skeletal muscle specifically alters the Ca(2+) channel function of the dihydropyridine receptor.Pflugers Archiv : European journal of physiology · 2008Article
- Evolution and modulation of intracellular calcium release during long-lasting, depleting depolarization in mouse muscle.The Journal of physiology · 2008Article
- Loss of caveolin-3 induced by the dystrophy-associated P104L mutation impairs L-type calcium channel function in mouse skeletal muscle cells.The Journal of physiology · 2007Article
- Transient loss of voltage control of Ca2+ release in the presence of maurocalcine in skeletal muscle.Biophysical journal · 2006Article
- Sarcoplasmic reticulum Ca2+ release and depletion fail to affect sarcolemmal ion channel activity in mouse skeletal muscle.The Journal of physiology · 2006Article
- Cross talk between Ca2+ and redox signalling cascades in muscle and neurons through the combined activation of ryanodine receptors/Ca2+ release channels.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2005Review
- Nitric oxide synthase inhibition affects sarcoplasmic reticulum Ca2+ release in skeletal muscle fibres from mouse.The Journal of physiology · 2005Article
- Both cGMP and peroxynitrite mediate chronic interleukin-6-induced negative inotropy in adult rat ventricular myocytes.The Journal of physiology · 2005Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In skeletal muscle, nitric oxide (NO) is commonly referred to as a modulator of the activity of the ryanodine receptor (RyR) calcium release channel. However the reported effects of NO on isolated sarcoplasmic reticulum (SR) preparations and single ryanodine receptor (RyR) activity are diverse, and how NO affects SR calcium release and intracellular calcium homeostasis under physiological conditions remains poorly documented and hardly predictable. Here, we studied the effects of NO donors on membrane current and intracellular [Ca(2+)] in single skeletal muscle fibres from mouse, under voltage-clamp conditions. When fibres were chronically exposed to millimolar levels of sodium nitroprusside (SNP) and challenged by short membrane depolarizations, there was a progressive increase in the resting [Ca(2+)] level. This effect was use-dependent with the slope of rise in resting [Ca(2+)] being increased two-fold when the depolarizing pulse level was raised from -20 to +10 mV. Analysis of the decay of the [Ca(2+)] transients suggested that cytoplasmic Ca(2+) removal processes were largely unaffected by the presence of SNP. Also the functional properties of the dihydropyridine receptor were very similar under control conditions and in the presence of SNP. The resting [Ca(2+)] elevation due to SNP was accompanied by a depression of the peak calcium release elicited by pulses to +10 mV. The effects of SNP could be reproduced by the chemically distinct NO donor NOC-12. They could be reversed upon exposure of the fibres to the thiol reducing agent dithiothreitol. Results suggest that large levels of NO produce a redox-sensitive continuous leak of Ca(2+) from the SR, through a limited number of release channels that do not close once they are activated by membrane depolarization. This SR Ca(2+) leak and the resulting increase in resting [Ca(2+)] may be important in mediating the effects of excess NO on voltage-activated calcium release.
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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.