Ca2+-dependent K+ transport in the Ehrlich ascites tumor cell.
The possible presence and properties of the Ca2+-dependent K+ channel have been investigated in the Ehrlich ascites tumor cell. The treatment with ionophore A23187 + CA2+, propranolol or the electron donor system ascorbate-phenazine methosulphate, all of which activate that transport system in the human erythrocyte, produces in the Ehrlich cell a net loss of K+ (balanced by the uptake of Na+) and a stimulation of both the influx and the efflux of 86Rb. These effects were antagonized by quinine, a known inhibitor of the Ca2+-dependent K+ channel in other cell systems, and by the addition of EGTA to the incubation medium. Ouabain did not have an inhibitory effect. These results suggests that the Ehrlich cell possesses a Ca2+-dependent K+ channel whose characteristics are similar to those described in other cell systems.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology*; D002286:Carcinoma, Ehrlich Tumor / Q000378:metabolism*; D002712:Chlorides / Q000378:metabolism; D004579:Electron Transport; D007473:Ion Channels / Q000187:drug effects; D007700:Kinetics; D051379:Mice; D011188:Potassium / Q000378:metabolism*; D011433:Propranolol / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism
D002712:Chlorides; D007473:Ion Channels; D000001:Calcimycin; D012964:Sodium; D011433:Propranolol; D011188:Potassium; D002118:Calcium