Increase in plasma potassium concentration following indomethacin administration: absence of a role for membrane Na-K ATPase

To elucidate whether indomethacin-induced hyperkalaemia is due to an inhibition of Na-K ATPase in the membranes, indomethacin (25 mg t.d.s.) was administered to 7 normal subjects for 7 days. This resulted in an increase in plasma potassium concentrations in all 7 subjects: median (range) for the entire group increased from 4.19 (3.98-4.79) mmol/l to 4.29 (4.13-4.87) mmol/l. Leucocytes preparred from these subjects prior to and after indomethacin were tested for⁸⁶Rb influx and [³H]-ouabain binding (an index of Na-K ATPase sites). Neither⁸⁶Rb influx (total, ouabain sensitive and ouabain insensitive) nor [³H]-ouabain binding changed significantly following indomethacin. We conclude that (a) indomethacin-induced hyperkalaemia is not due to alterations in potassium influx into cells and (b) the modulation of Na-K ATPase sites/activity is in leucocytes not dependent upon prostaglandins.