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Am J Physiol Lung Cell Mol Physiol (October 26, 2001). doi:10.1152/ajplung.00142.2001
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Articles in PresS, published online ahead of print October 26, 2001
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00142.2001
Submitted on April 24, 2001
Accepted on October 23, 2001

ß-adrenoceptor mediated control of apical membrane conductive properties in fetal distal lung epithelia

Andrew Collett1, Sarah J Ramminger1, Richard E Olver1, and Stuart M Wilson1*

1 University of Dundee, Tayside Institute of Child Health, Dundee, Tayside, United Kingdom

* To whom correspondence should be addressed. E-mail: S.M.Wilson{at}dundee.ac.uk.

Distal lung epithelial cells isolated from fetal rats were cultured (48 h) on permeable supports so that transepithelial ion transport could be quantified electrometrically. Unstimulated cells generated a short circuit current (ISC) that was inhibited (~80%) by apical amiloride. The current is thus due, predominantly, to the absorption of Na+ from the apical solution. Isoprenaline increased the amiloride-sensitive ISC ~2 fold. Experiments in which apical membrane Na+ currents were monitored in basolaterally-permeabilised cells showed that this was accompanied by a rise apical Na+ conductance (GNa+). Isoprenaline also increased apical Cl- conductance (GCll-) by activating an anion channel species sensitive to glibenclamide but unaffected by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS). The isoprenaline-evoked changes in GNa+ and GCl- could account for the changes in ISC observed in intact cells. Glibenclamide had no effect upon the isoprenaline-evoked stimulation of ISC or GNa+ demonstrating that the rise in GCl- is not essential to the stimulation of Na+ transport.




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