Chloride Transport by Gastric Mucosa

Forte, John G.; Reenstra, William W.

doi:10.1007/978-3-642-78261-9_13

Cited by 4 publications

(3 citation statements)

References 45 publications

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“…Third, CFTR has a relatively low conductance to HCO 3 Ϫ (15). In the proposed model ( 18), basolateral Cl Ϫ / HCO 3 Ϫ exchange is used to concentrate intracellular Cl Ϫ concentration above the Cl Ϫ equilibrium potential (6,13,20,22).…”

mentioning

confidence: 99%

Evidence that Calu-3 human airway cells secrete bicarbonate

Lee

Penland

Widdicombe

et al. 1998

American Journal of Physiology-Lung Cellular and Molecular Phys

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The Calu-3 cell line is being investigated as a model for human submucosal gland serous cells. In a previous investigation of basal short-circuit current ( I sc) in Calu-3 cells, high levels of bumetanide-insensitive basal I sc (∼60 μA/cm2) were measured in cells grown at an air interface. Basal I sc was reduced only 7% by bumetanide, and the largest component of basal I sc required both Cl− and[Formula: see text] in the bathing solutions. Because I sc could be partially inhibited by basolateral 4,4′-dinitrostilbene-2,2′-disulfonic acid and because the only known apical exit pathway for anions is the cystic fibrosis transmembrane conductance regulator, which has a relatively poor conductance for [Formula: see text], it was concluded that most basal I sc is[Formula: see text]-dependent Cl− secretion [M. Singh, M. Krouse, S. Moon, and J. J. Wine. Am. J. Physiol. 272 ( Lung Cell. Mol. Physiol. 16): L690–L698, 1997]. We have now measured isotopic fluxes of36Cl−and22Na+across short-circuited Calu-3 cells and found that virtually none of the basal I sc is Cl− secretion or Na+ absorption. Thus, in contrast to the earlier report, we conclude that the major component of basal I sc is[Formula: see text] secretion. Stimulation recruits primarily Cl− secretion, as previously proposed.

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mentioning

confidence: 99%

Evidence that Calu-3 human airway cells secrete bicarbonate

Lee

Penland

Widdicombe

et al. 1998

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…4D). This would be an expected response in Cl Ϫ -free conditions, because parietal cell acidic and nonacidic Cl Ϫ secretion is inhibited, which greatly affects (increases) TER (6). Exposure of tissues treated with Cl Ϫ -free solutions to 1 M NaCl for 10 min induced an immediate decrease in TER (Fig.…”

Section: Resultsmentioning

confidence: 92%

Restitution of the bullfrog gastric mucosa is dependent on a DIDS-inhibitable pathway not related to \batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(\mathrm{HCO}_{3}^{-}\) \end{document} ion transport

Hagen

Morrison

Law

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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This study was conducted to determine the contribution of ion transport to restitution after injury in the gastric mucosa. For this, intact sheets of stomach from the bullfrog, Rana catesbeiana, were mounted in Ussing chambers. Restitution was evaluated in the presence or absence of ion transport inhibitors amiloride, DIDS, and bumetanide to block Na(+)/H(+) exchange, Cl(-)/HCO(3)(-) exchange and Na(+)/HCO(3)(-) co-transport, and Na(+)-K(+)-2Cl(-) cotransport, respectively. Ion substitution experiments with Na(+)-free, Cl(-)-free, and HCO(3)(-)-free solutions were also performed. Injury to the mucosa was produced with 1 M NaCl, and restitution was evaluated by recovery of transepithelial resistance (TER), mannitol flux, and morphology. Amiloride, bumetanide, Cl(-)-free, or HCO(3)(-)-free solutions did not affect restitution. In Na(+)-free solutions, recovery of TER and mannitol flux did not occur because surface cells did not attach to the underlying basement membrane. In contrast, all aspects of restitution were inhibited by DIDS, a compound that inhibits Na(+)-dependent HCO(3)(-) transport. Because HCO(3)(-)-free solutions did not inhibit restitution, it was concluded that DIDS must block a yet undefined pathway not involved in HCO(3)(-) ion transport but essential for cell migration after injury and restitution in the gastric mucosa.

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“…In addition to numerous basolateral K ϩ channels that recycle K ϩ imported by Na ϩ -K ϩ -ATPase, it is thought that oxyntic and parietal cells possess an apical K ϩ channel(s) that is (are) active only during acid secretion. The apical K ϩ channel facilitates the movement of cytoplasmic K ϩ into the gastric lumen; K ϩ is then recycled back into the cell by H ϩ -K ϩ -ATPase activity during acid secretion (7). In a preliminary report by Horio et al (13), it was determined that the apical membrane of stimulated parietal cells has an inwardly rectifying K ϩ channel (Kir4.1).…”

Section: Discussionmentioning

confidence: 99%

NH₄Cl inhibition of acid secretion: possible involvement of an apical K⁺channel in bullfrog oxyntic cells

Hagen

Morrison

2000

American Journal of Physiology-Gastrointestinal and Liver Physi

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This study was undertaken to determine the mechanism by which ammonium chloride (NH(4)Cl) inhibits stimulated acid secretion in the bullfrog gastric mucosa. To this end, four possible pathways of inhibition were studied: 1) blockade of basolateral K(+) channel, 2) blockade of ion transport activity, 3) neutralization of secreted H(+) in the luminal solution, or 4) ATP depletion. Addition of nutrient 10 mM NH(4)Cl (calculated NH(3) concentration = 92.5 microM and NH(4)(+) concentration = 9.91 mM) inhibited acid secretion within 30 min. Inhibition of acid secretion did not occur by blockade of basolateral K(+) channel activity or ion transport activity or by neutralization of the luminal solution. Although ATP depletion occurred in the presence of NH(4)Cl, the magnitude of ATP depletion in 30 min was not sufficient to inhibit stimulated acid secretion. By comparing the effect of NH(4)Cl on the resistance of inhibited or stimulated tissues, we demonstrate that NH(4)Cl acts specifically on stimulated tissues. We propose that NH(4)Cl blocks activity of an apical K(+) channel present in stimulated oxyntic cells. Our data suggest that the activity of this channel is important for the regulation of acid secretion in bullfrog oxyntic cells.

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Chloride Transport by Gastric Mucosa

Cited by 4 publications

References 45 publications

Evidence that Calu-3 human airway cells secrete bicarbonate

Evidence that Calu-3 human airway cells secrete bicarbonate

NH₄Cl inhibition of acid secretion: possible involvement of an apical K⁺channel in bullfrog oxyntic cells

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Chloride Transport by Gastric Mucosa

Cited by 4 publications

References 45 publications

Evidence that Calu-3 human airway cells secrete bicarbonate

Evidence that Calu-3 human airway cells secrete bicarbonate

NH4Cl inhibition of acid secretion: possible involvement of an apical K+channel in bullfrog oxyntic cells

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NH₄Cl inhibition of acid secretion: possible involvement of an apical K⁺channel in bullfrog oxyntic cells