1. Extracellular K+ activity in frog ventricular muscle was monitored with a K+-selective micro-electrode during and following periods of rapid stimulation. 2. During activity K+ accumulated in the paracellular space, declined with continued beating and became depleted below bathing K+ concentrations, [K+], when activity was terminated. 3. The re-uptake and depletion of K+ was inhibited by ouabain, Li+ and lowering bathing [K+], and was enhanced by prolonged stimulation, raising bathing [K+], and by addition of adrenaline. These ionic and drug dependencies of the K+ re-uptake process are similar to the ionic and drug dependencies of the Na+-K+-ATPase system. 4. Frequency-induced K+ accumulation appears to result from a delay in the activation of the Na+ pump. 5. Possible changes in intracellular sodium concentration, [Na+]i, in the response to changes in frequency, appear to be a more powerful stimulant of the K+ re-uptake process than changes in extracellular potassium concentration, [K+]o. 6. Frequency-induced changes in [K+]o were also detected by measurements of resting potential. Alterations in membrane potential and action potential duration observed during and following electrical stimulation are suggestive of an electrogenic K+ re-uptake process. 7. Aside from their direct effects on the action potential, Ca2+ and Mg2+ had little or no effect on Na+ pump activity. While Ni2+ suppressed pump activity, Ba2+ indirectly enhanced the K+ uptake process by blocking the resting K+ conductance. 8. K+ uptake rate was estimated to range between 3 and 8 p-mole/cm2.sec. Since diffusion in and out of the paracellular space was a much slower process (t1/2 60-90 sec), it contributes little to the beat-to-beat control of paracellular [K+].