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 (I sc) 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 I sc 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 (G Na+). Isoprenaline also increased apical Cl- conductance (G Cl-) by activating an anion channel species sensitive to glibenclamide but unaffected by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS). The isoprenaline-evoked changes inG Na+ and G Cl-could account for the changes in I sc observed in intact cells. Glibenclamide had no effect upon the isoprenaline-evoked stimulation of I sc orG Na+ demonstrating that the rise inG Cl- is not essential to the stimulation of Na+ transport.
|Number of pages||10|
|Journal||American Journal of Physiology: Lung Cellular and Molecular Physiology|
|Publication status||Published - 2002|
- Alveolar ion transport
- Ussing chambers
- Permeabilized epithelia