A maxi calcium-activated potassium channel from chick lens epithelium.

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(-7) M. 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 greater than .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.