Furosemide‐sensitive potassium efflux in cultured mouse fibroblasts

Transfer of LM(TK − ) cells from normal growth medium to medium lacking K + leads to a rapid loss of intracellular K + , which is 50–70% inhibited by furosemide or bumetanide. The diuretic‐sensitive component of K + efflux requires both Na + and Cl − , and is presumably mediated by a K + , Na + , Cl − cotransport system of the kind described in avian erythrocytes and Ehrlich ascites cells. It can be calculated that such a system should be near equilibrium under normal growth conditions but should mediate net efflux (as observed) when the driving force is altered by reducing extracellular K + . The diuretic‐sensitive component of net K + efflux is also sensitive to amiloride. This effect is probably indirect, however, with amiloride acting to block the Na + influx that supplies Na + to the cotransport system. At the low extracellular K + concentrations employed in these studies, the diuretic‐sensitive system is a physiologically important pathway of K + loss. The rate of growth in low‐K + medium can be increased (or the rate of cell lysis decreased) by adding diuretic or by reducing external Na + or Cl − .