ArticleThe Journal of physiology2005
Nitric oxide synthase inhibition affects sarcoplasmic reticulum Ca2+ release in skeletal muscle fibres from mouse.
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 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Have We Looked in the Wrong Direction for More Than 100 Years? Delayed Onset Muscle Soreness Is, in Fact, Neural Microdamage Rather Than Muscle Damage.Antioxidants (Basel, Switzerland) · 2020Article
- Neuroprotective mechanism of low-dose sodium nitrite in oxygen-glucose deprivation model of cerebral ischemic stroke in PC12 cells.EXCLI journal · 2019Article
- Improved tolerance of acute severe hypoxic stress in chronic hypoxic diaphragm is nitric oxide-dependent.The journal of physiological sciences : JPS · 2015Article
- Depression of voltage-activated Ca2+ release in skeletal muscle by activation of a voltage-sensing phosphatase.The Journal of general physiology · 2015Article
- Phosphoinositide substrates of myotubularin affect voltage-activated Ca²⁺ release in skeletal muscle.Pflugers Archiv : European journal of physiology · 2014Article
- Modulation of contractile apparatus Ca2+ sensitivity and disruption of excitation-contraction coupling by S-nitrosoglutathione in rat muscle fibres.The Journal of physiology · 2011Article
- Acute effects of reactive oxygen and nitrogen species on the contractile function of skeletal muscle.The Journal of physiology · 2011Review
- In vivo expression of G-protein beta1gamma2 dimer in adult mouse skeletal muscle alters L-type calcium current and excitation-contraction coupling.The Journal of physiology · 2010Article
- T-tubule disorganization and defective excitation-contraction coupling in muscle fibers lacking myotubularin lipid phosphatase.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- 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
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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
Nitric oxide (NO) generated by skeletal muscle is believed to regulate force production but how this is achieved remains poorly understood. In the present work we tested the effects of NO synthase (NOs) inhibitors on membrane current and intracellular calcium in isolated skeletal muscle fibres from mouse, under voltage-clamp conditions. Resting [Ca(2+)] and [Ca(2+)] transients evoked by large depolarizations exhibited similar properties in control fibres and in fibres loaded with tenth millimolar levels of the NOs inhibitor N-nitro-L-arginine (L-NNA). Yet the voltage dependence of calcium release was found to be shifted by approximately 15 mV towards negative values in the presence of L-NNA. This effect could be reproduced by the other NOs inhibitor S-methyl-L-thiocitrulline (L-SMT). Separate experiments showed that the voltage dependence of charge movement and of the slow calcium current were unaffected by the presence of L-NNA, ruling out an effect on the voltage sensor. A negative shift in the voltage dependence of calcium release with no concurrent alteration in the properties of charge movement was also observed in fibres exposed to the oxidant H(2)O(2) (1 mM). Conversely the reducing agent dithiothreitol (10 mM) had no obvious effect on Ca(2+) release. Overall, the results indicate that physiological levels of NO exert a tonic inhibitory control on the activation of the calcium release channels. Changes in the voltage dependence of Ca(2+) release activation may be a ubiquitous physiological consequence of redox-related modifications of the ryanodine receptor.
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