ArticleJournal of muscle research and cell motility1998
Sodium nitroprusside, a NO donor, modifies Ca2+ transport and mechanical properties in frog skeletal muscle.
Article in Journal of muscle research and cell motility, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 28 citations in OpenAlex.
- 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
- Relationship between human aging muscle and oxidative system pathway.Oxidative medicine and cellular longevity · 2012Review
- Reactive oxygen species: impact on skeletal muscle.Comprehensive Physiology · 2011Review
- Regulation of fast skeletal muscle activity by SERCA1 vicinal-cysteines.Journal of muscle research and cell motility · 2009Article
- Exercise-induced oxidative stress: cellular mechanisms and impact on muscle force production.Physiological reviews · 2008Review
- Specific correlations between muscle oxidative stress and chronic fatigue syndrome: a working hypothesis.Journal of muscle research and cell motility · 2007Review
- Age and sex influence on oxidative damage and functional status in human skeletal muscle.Journal of muscle research and cell motility · 2001Article
- Modifications of Ca2+ transport induced by glutathione in sarcoplasmic reticulum membranes of frog skeletal muscle.Journal of muscle research and cell motility · 2000Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently it has been hypothesized that, in skeletal muscle, NO produced directly by high-frequency stimulation could produce contraction through reactions with thiol groups on the sarcoplasmic reticulum (SR). However, a possible cGMP-mediated relaxing effect, similar to that seen in smooth muscle, has also been demonstrated. We used purified SR preparations and single fibres from frog fast muscles incubated with different concentrations of sodium nitroprusside (SNP) in this study. The results obtained from a long low-frequency stimulation, together with those from a study on Ca2+ transport regulation, showed that the presence of NO precursor induced: an acceleration of the onset of fatigue in single fibres; a decreased vesicular Ca2+ content due to increased Ca2+ release; a shift to open status in SR Ca2+ channels; an increase in SR Ca2+ pump activity. The data presented in this paper seem to indicate that the increased NO in the muscle fibres can influence muscle activity in different ways, perhaps depending on the metabolic status of the muscle and target (filaments, sarcolemma, SR) with which the NO (or its derivatives) acts.
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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.