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The effect of the sulphydryl reagent N-ethylmaleimide on the K+ and Cl- transport pathways of the lamprey erythrocyte membrane was found to be quite complex. N-Ethylmaleimide inhibited the Ba(2+)-sensitive pathway that mediates most of the ouabain-resistant influx of K+ into the cell under physiological conditions but stimulated a Cl(−)-dependent, B(2+)-resistant K+ transport pathway that was inhibited by compounds that inhibit Cl(−)-dependent K+ transport in the human erythrocyte. N-Ethylmaleimide (in most cases) reduced the total influx of Cl- into the lamprey erythrocyte but (in all cases) introduced a K(+)-dependent component into the measured Cl- uptake; this was explained in terms of N-ethylmaleimide having inhibited the pathway primarily responsible for Cl- influx under physiological conditions but having stimulated a second, K(+)-dependent Cl- transport pathway. Although the magnitude of the K+ and Cl- fluxes stimulated by N-ethylmaleimide varied widely between cells from different lampreys, there was, in each individual case, a close similarity between the magnitude of the Cl(−)-dependent K+ influx (calculated from the 86Rb+ uptake) and the K(+)-dependent Cl- influx; the mean value for the ratio of the former to the latter was 1.01 +/− 0.03 (N = 5). The results are therefore consistent with the sulphydryl reagent having activated a K+/Cl- cotransport system similar to that present in erythrocytes from many mammalian species. This raises the possibility that the lamprey red cell may be a uniquely suitable system in which to study the characteristics of Cl- transport by this pathway.

The effect of N-ethylmaleimide on K+ and Cl- transport pathways in the lamprey erythrocyte membrane: activation of K+/Cl- cotransport