BENZAMIL-INDUCED CONDUCTIVE STATE OF INSULIN-STIMULATED, AMILORIDE-BLOCKABLE CATION CHANNEL IN FETAL LUNG EPITHELIUM

Insulin activated a 28 pS amiloride-blockable nonselective cation (NSC) channel in rat fetal distal lung epithelium. Benzamil, an analogue of amiloride, decreased the open probability (P-o) of the insulin-unstimulated channel from 0.06+/-0.02 to 0.0013+/-0.0006 (mean+/-SEM, n=5-7; 100 mu M benzamil application to extracellular surface), but increased the P-o of the insulin-stimulated channel from 0.10+/-0.02 to 0.69+/-0.02 (mean+/-SEM, n = 5-7; 100 mu M benzamil application to extracellular surface). The effects of benzamil could be observed in either case that it was applied to the extracellular or cytosolic surface. Unlike benzamil, amiloride decreased the P-o of both insulin-unstimulated and -stimulated channels. These observations suggest that benzamil acts as a blocker on the insulin-unstimulated NSC channel but as an opener on the insulin-stimulated NSC channel.