Abstract
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-inducedIo but enhanced the amplitude markedly. The CNIo 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 thatIo is due to the activation of Ca2+-dependent K+ channels. Consistent with this notion, the Ca2+-mobilizing agents, muscarine and caffeine, also producedIo. Exposure to CN in a Ca2+-deficient medium for 4 min abolished caffeine- or muscarine-inducedIo without development ofIo, and addition of Ca2+ to the CN-containing solution inducedIo. We conclude that exposure to CN produces Ca2+-dependent K+ currents in an external Ca2+-dependent manner, probably via facilitation of Ca2+ influx.