The apical membrane of embryonic chick lens epithelium contains at high density, a large conductance K+channel whose open probability is increased by Ca++at the inner surface of the membrane and by depolarization. The conductance of the channel when it is fully open in symmetrical 150 mM K+solutions is 214±3 pS (mean±std. error). The current through the channel is a function of the K+concentration. Gating (open probability) at positive transmembrane voltages increases as the internal [Ca++] is raised above 10-7M. The open probability decreases monotonically as the transmembrane voltage is made more negative. The channel is at least 87 times more permeable to K+than to Na+or Li+and shows appreciable permeability to Rb+and NH4+. It has at least three subconductance levels amounting to approximately 3/4, 1/2, and 1/4 the fully open unitary conductance. The occurrence of these subconductance levels is highly variable from one patch to another. The channel is blocked by physiological levels of internal Na+but not over a physiological voltage range. This block is partially overcome by elevated external K+.This K+channel from chick lens epithelium is blocked by a number of compounds known to block BK channels in other tissues. Here we show that decamethonium and Ba++are effective blockers when added to the inner bathing solution at concentrations≥. 1 mM. Tetraethylammonium, Cs+, quinine, quinidine and Ba++are all effective blockers when applied to the outer side of the channel in the. 1 mM–5 mM range. With the exception of internal Ba++, all of these compounds produce a fast flicker-type blockade. We use a one-site model to quantify the blockade caused by these flicker producing agents. The voltage dependence of the blockade by Cs+suggests that this channel probably allows multiple occupancy.