Efflux of intracellular K
+ from human erythrocytes was stimulated under nonhemolytic conditions by each of four phenothiazine derivatives, two non-steroidal anti-inflammatory drugs and a local anesthetic, and was dependent on time and temperature, while membrane shape change induced by them was independent of time and temperature. Cepharanthine, one of biscoclaurine alkaloids, and lipid bilayer perturbing agents, such as lysolecithin, phospholipase A
2 and C, and quarternary ammonium compounds, induced membrane shape change without stimulating K
+ efflux at any temperature. In contrast, N-ethylmaleimide, membrane protein modifying reagent, remarkably stimulated K
+ efflux time- and temperature-dependently without inducing membrane shape change. These results suggest that the K
+ efflux may result from drug-induced rearrangement of a certain membrane protein (e.g. K
+-channel protein) and is independent of membrane shape change, which appears to result from the perturbation of membrane lipid bilayer.
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