Furosemide‐sensitive potassium efflux in cultured mouse fibroblasts

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Abstract
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−.