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-Adrenoceptor-mediated control of apical
membrane conductive properties in fetal distal lung
epithelia
Lung Membrane Transport Group, Tayside Institute of Child Health, Ninewells Hospital and Medical School, University of Dundee, Dundee DD1 9SY, United Kingdom
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 about twofold.
Experiments in which apical membrane Na+ currents were
monitored in basolaterally permeabilized cells showed that this was
accompanied by a rise in apical Na+ conductance
(GNa+). Isoprenaline also increased apical
Cl
conductance (GCl
) 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.
alveolar ion transport; Ussing chambers; permeabilized epithelia
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