Filipin, a polyene antibiotic known to induce leakage of materials from various cells, depresses K(+) and NO(3) (-) uptake in etiolated pea epicotyl segments. Filipin concentrations which strongly reduce K(+) influx have little effect on efflux; however, high concentrations enhance K(+) efflux. Filipin has no effect on respiration rates or cell electropotentials; its action is presumed to be on the cell membranes. Cholesterol, but not a thiol-protecting agent (dithiothreitol), enhances K(+) influx and counteracts the inhibition by filipin. Although this effect of cholesterol may be due to an interaction with filipin in the outer solution, there is reason to believe that its major effect is to impart stability to the membrane; filipin is believed to act by interfering with sterol stabilization of phospholipid layers. The predominant native sterols of etiolated pea stem (Pisum sativum L. var. Alaska), which cholesterol probably mimics, are beta-sitosterol, campesterol, and stigmasterol.