We have studied the effect on K transport of reductions in the Na and Cl concentrations of solutions perfusing the isolated bullfrog kidney. We used recently developed techniques for estimating the unidirectional reabsorptive and secretory K fluxes. Reduction of Na and Cl concentrations in the arterial perfusate from 112 and 100 mM to 22 and 10 mM, respectively, inhibited K secretion 82% and K reabsorption 97%. Reduction of only the Na concentration inhibited K secretion 42% but did not affect K reabsorption. Arterial and portal perfusion with 37 mM Na, 23 mM Cl reduced urine Na concentration to 6 mM and Na reabsorption by 59%. However, K secretion rose 88% and reabsorption fell 76%. Arterial and portal perfusates with 37 mM Na, 100 mM Cl reduced urine Na concentration to 2 mM and Na reabsorption by 46%. Still, K secretion was elevated 57% by an increase in urine flow rate. K reabsorption was not reduced. Arterial and portal perfusates with 112 mM Na, 23 mM Cl, and containing SO4 also stimulated K secretion 26% and inhibited K reabsorption 91%. Thus, reduction of perfusate Na concentration to 22 mM inhibited secretion but 37 mM was sufficient to permit stimulation of secretion by low Cl concentrations and by increased tubular fluid flow rate. Reduction of the perfusate Cl concentration stimulated secretion and inhibited reabsorption. We conclude that a minimum level of Na reabsorption is required to maintain K secretion, but above that minimum level changes in the rate of Na reabsorption do not affect the rate of K secretion. The tubular fluid Cl concentration or the rate of Cl reabsorption affects both reabsorption and secretion of K and, therefore, may be an important regulator of the rate of K excretion.