Activation of Ca(2+)-dependent K+ channels by cyanide in guinea pig adrenal chromaffin cells.

The effects of cyanide (CN) on whole cell current measured with the perforated-patch method were studied in adrenal medullary cells. Application of CN produced initially inward and then outward currents at -52 mV or more negative. As the membrane potential was hyperpolarized, amplitude and latency of the outward current (Io) by CN became small and long, respectively. A decrease in the external Na+ concentration did not affect the latency for CN-induced Io but enhanced the amplitude markedly. The CN Io reversed polarity at -85 mV, close to the Nernst potential for K+, and was suppressed by the K+ channel blockers curare and apamin but not by glibenclamide, suggesting that Io is due to the activation of Ca(2+)-dependent K+ channels. Consistent with this notion, the Ca(2+)-mobilizing agents, muscarine and caffeine, also produced Io. Exposure to CN in a Ca(2+)-deficient medium for 4 min abolished caffeine- or muscarine-induced Io without development of Io, and addition of Ca2+ to the CN-containing solution induced Io. We conclude that exposure to CN produces Ca(2+)-dependent K+ currents in an external Ca(2+)-dependent manner, probably via facilitation of Ca2+ influx.