Beta-Adrenoceptor-mediated control of apical membrane conductive properties in fetal distal lung epithelia

Collett, Andrew, Ramminger, S.J., Olver, R.E. and Wilson, S.M. (2002) Beta-Adrenoceptor-mediated control of apical membrane conductive properties in fetal distal lung epithelia. American journal of physiology - Lung cellular and molecular physiology, 282 (4). L621-L630. ISSN 1040-0605

Abstract

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.

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