ArticlePloS one2012
Chronic nicotine modifies skeletal muscle Na,K-ATPase activity through its interaction with the nicotinic acetylcholine receptor and phospholemman.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Rhabdomyolysis Following Rapid Correction of Acute Hyponatraemia in a Patient With Psychogenic Polydipsia.Cureus · 2026Article
- AMPK and glucose deprivation exert an isoform-specific effect on the expression of NaJournal of muscle research and cell motility · 2024Article
- Exercise and fatigue: integrating the role of KEuropean journal of applied physiology · 2023Review
- E-cigarette aerosol impairs male mouse skeletal muscle force development and prevents recovery from injury.American journal of physiology. Regulatory, integrative and comparative physiology · 2022Article
- Chronic Ouabain Prevents Radiation-Induced Reduction in the α2 Na,K-ATPase Function in the Rat Diaphragm Muscle.International journal of molecular sciences · 2022Article
- Angiotensin 1-7 prevents the excessive force loss resulting from 14- and 28-day denervation in mouse EDL and soleus muscle.The Journal of general physiology · 2021Article
- The role of AMPK in regulation of NaJournal of muscle research and cell motility · 2021Review
- Article
- Ouabain Suppresses IL-6/STAT3 Signaling and Promotes Cytokine Secretion in Cultured Skeletal Muscle Cells.Frontiers in physiology · 2020Article
- AMP-Activated Protein Kinase as a Key Trigger for the Disuse-Induced Skeletal Muscle Remodeling.International journal of molecular sciences · 2018Review
- Pivotal role of α2 NaThe Journal of physiology · 2016Review
- High oxygen extraction and slow recovery of muscle deoxygenation kinetics after neuromuscular electrical stimulation in COPD patients.European journal of applied physiology · 2016Article
- Distinct α2 Na,K-ATPase membrane pools are differently involved in early skeletal muscle remodeling during disuse.The Journal of general physiology · 2016Article
- Specialized Functional Diversity and Interactions of the Na,K-ATPase.Frontiers in physiology · 2016Review
- Phospholemman is not required for the acute stimulation of Na⁺-K⁺-ATPase α₂-activity during skeletal muscle fatigue.American journal of physiology. Cell physiology · 2015Article
- Understanding the physiology of the asymptomatic diaphragm of the M1592V hyperkalemic periodic paralysis mouse.The Journal of general physiology · 2015Article
- Na,K-ATPase α2 activity in mammalian skeletal muscle T-tubules is acutely stimulated by extracellular K+.The Journal of general physiology · 2015Article
- Functional interaction of nicotinic acetylcholine receptors and Na+/K+ ATPase from Locusta migratoria manilensis (Meyen).Scientific reports · 2015Article
- Isoform-specific Na,K-ATPase alterations precede disuse-induced atrophy of rat soleus muscle.BioMed research international · 2015Article
- Musculoskeletal disorders in chronic obstructive pulmonary disease.BioMed research international · 2014Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous finding that the muscle nicotinic acetylcholine receptor (nAChR) and the Na,K-ATPase interact as a regulatory complex to modulate Na,K-ATPase activity suggested that chronic, circulating nicotine may alter this interaction, with long-term changes in the membrane potential. To test this hypothesis, we chronically exposed rats to nicotine delivered orally for 21-31 days. Chronic nicotine produced a steady membrane depolarization of ∼3 mV in the diaphragm muscle, which resulted from a net change in electrogenic transport by the Na,K-ATPase α2 and α1 isoforms. Electrogenic transport by the α2 isoform increased (+1.8 mV) while the activity of the α1 isoform decreased (-4.4 mV). Protein expression of Na,K-ATPase α1 or α2 isoforms and the nAChR did not change; however, the content of α2 subunit in the plasma membrane decreased by 25%, indicating that its stimulated electrogenic transport is due to an increase in specific activity. The physical association between the nAChR, the Na,K-ATPase α1 or α2 subunits, and the regulatory subunit of the Na,K-ATPase, phospholemman (PLM), measured by co-immuno precipitation, was stable and unchanged. Chronic nicotine treatment activated PKCα/β2 and PKCδ and was accompanied by parallel increases in PLM phosphorylation at Ser(63) and Ser(68). Collectively, these results demonstrate that nicotine at chronic doses, acting through the nAChR-Na,K-ATPase complex, is able to modulate Na,K-ATPase activity in an isoform-specific manner and that the regulatory range includes both stimulation and inhibition of enzyme activity. Cholinergic modulation of Na,K-ATPase activity is achieved, in part, through activation of PKC and phosphorylation of PLM.
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