ArticlePflugers Archiv : European journal of physiology2006
Nucleotide regulation of paracellular Cl- permeability in natural rabbit airway epithelium.
Article in Pflugers Archiv : European journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 13 citations in OpenAlex.
- A spatial model of fluid recycling in the airways of the lung.Journal of theoretical biology · 2015Article
- Biophysical model of ion transport across human respiratory epithelia allows quantification of ion permeabilities.Biophysical journal · 2013Article
- P2Y2 receptor knock-out mice display normal NaCl absorption in medullary thick ascending limb.Frontiers in physiology · 2013Article
- Function of Proton Channels in Lung Epithelia.Wiley interdisciplinary reviews. Membrane transport and signaling · 2012Article
- Ion transport regulation by P2Y receptors, protein kinase C and phosphatidylinositol 3-kinase within the semicircular canal duct epithelium.BMC research notes · 2010Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we demonstrate a novel regulatory mechanism by which mucosal nucleotides via P2Y receptors decrease paracellular Cl(-) ion permeability in natural rabbit airway epithelium (in addition to a decrease in active Na(+) absorption). In contrast to primary cultures, the natural airway epithelium is a low-resistance epithelium, and an equivalent circuit model predicts that changes of more than approximately 12% in transepithelial conductance (G (t)) must include an effect on paracellular conductance (G (s)). Mucosal P2Y receptor stimulation with uridine triphosphate (UTP; 200 microM) decreased G (t) by up to 50% (average, 24%) and simultaneously decreased the paracellular Cl(-) permeability (mucosa-to-serosa Cl(-) flux) by 16%, but had no effect on mannitol permeability. The G (t) response to UTP was mimicked and attenuated by ionomycin (1 microM), suggesting a dependence on Ca(2+) (i). Amiloride (100 microM) and hyperosmolarity (+75 mM mannitol) also decreased G (t), indicating a role of cell shrinkage. Elevation of cAMP with forskolin (8 microM) or isoproterenol (10 microM) increased G (t) by 55 and 32%, and forskolin increased paracellular Cl(-) permeability by 37% without affecting mannitol permeability. The opposite effects of Ca(2+) (i) and cAMP on G (t) suggest an autocrine nucleotide signaling sequence where P2Y-dependent decrease in passive, paracellular Cl(-) transport is succeeded by a reversion of this effect due to P1-receptor-stimulated cAMP formation by adenosine originating from a time-dependent breakdown of mucosal ATP.
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