ArticleAmerican journal of physiology. Lung cellular and molecular physiology2013
Cholinergic regulation of epithelial sodium channels in rat alveolar type 2 epithelial cells.
Article in American journal of physiology. Lung cellular and molecular physiology, 2013. 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, 24 citations in OpenAlex.
- Rescue of alveolar wall liquid secretion blocks fatal lung injury due to influenza-staphylococcal coinfection.The Journal of clinical investigation · 2023Article
- Activation of Endothelial Large Conductance Potassium Channels Protects against TNF-α-Induced Inflammation.International journal of molecular sciences · 2023Article
- Article
- Enhanced epithelial sodium channel activity in neonatal Scnn1b mouse lung attenuates high oxygen-induced lung injury.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Ion channels of the lung and their role in disease pathogenesis.American journal of physiology. Lung cellular and molecular physiology · 2017Review
- Cytokine-Ion Channel Interactions in Pulmonary Inflammation.Frontiers in immunology · 2017Review
- Inhibition of airway surface fluid absorption by cholinergic stimulation.Scientific reports · 2016Article
- Role of epithelial sodium channels in the regulation of lung fluid homeostasis.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Respiratory complications of organophosphorus nerve agent and insecticide poisoning. Implications for respiratory and critical care.American journal of respiratory and critical care medicine · 2014Review
- Chronic ethanol exposure alters the lung proteome and leads to mitochondrial dysfunction in alveolar type 2 cells.American journal of physiology. Lung cellular and molecular physiology · 2014Article
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Authors and funding
8 authors at 1 institution in 2 countries.
Funding
Abstract
We and others have shown that epithelial Na(+) channels (ENaC) in alveolar type 2 (AT2) cells are activated by β2 agonists, steroid hormones, elevated oxygen tension, and by dopamine. Although acetylcholine receptors (AChRs) have been previously described in the lung, there are few reports of whether cholinergic agonists alter sodium transport in the alveolar epithelium. Therefore, we investigated how cholinergic receptors regulate ENaC activity in primary cultures of rat AT2 cells using cell-attached patch-clamp recordings to assess ENaC activity. We found that the muscarinic agonists, carbachol (CCh) and oxotremorine, activated ENaC in a dose-dependent manner but that nicotine did not. CCh-induced activation of ENaC was blocked by atropine. Western blotting and immunohistochemistry suggested that muscarinic M2 and M3 receptors (mAChRs) but not nicotinic receptors were present in AT2 cells. Endogenous RhoA and GTP-RhoA increased in response to CCh and the increase was reduced by pretreatment with atropine. We showed that Y-27632, an inhibitor of Rho-associated protein kinase (ROCK), abolished endogenous ENaC activity and inhibited the activation of ENaC by CCh. We also showed that ROCK signaling was necessary for ENaC stability in 2F3 cells, a model for AT2 cells. Our results showed that muscarinic agonists activated ENaC in rat AT2 cells through M2 and/or M3 mAChRs probably via a RhoA/ROCK signaling pathway.
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