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.
|Number of pages
|American Journal of Physiology - Lung Cellular and Molecular Physiology
|Early online date
|1 Apr 2002
|Published - 1 Apr 2002