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 o f amiloride, decreased the open probability (P-o) of the insulin-unsti mulated 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 increas ed 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 extracel lular surface). The effects of benzamil could be observed in either ca se that it was applied to the extracellular or cytosolic surface. Unli ke benzamil, amiloride decreased the P-o of both insulin-unstimulated and -stimulated channels. These observations suggest that benzamil act s as a blocker on the insulin-unstimulated NSC channel but as an opene r on the insulin-stimulated NSC channel.