The mechanism of secretory supply of K⁺ into the diluting segment of nephron was studied in Triturus kidneys by observing Ba²⁺ effects on electrical phenomena related to K⁺ movements and other electrical properties of the segment. Ba²⁺ (1-2mM) applied into the luminal fluid completely blocked K⁺ movement into the lumen during the stop-flow of the intraluminal K⁺-free solution. Also, Ba²⁺ inhibited transepithelial K⁺ diffusion potential induced by alterations in the intraluminal K⁺ concentration and increased transtubular resistance (R_t). A rapidly decaying time course of the K⁺ diffusion potential and its high peak amplitude (near the maximum expected from an imposed concentration difference) suggest that the diffusion potential was generated across the paracellular pathways. Step-changes in the Na⁺ concentration induced similar but smaller diffusion potentials, which were also inhibited by Ba²⁺. Replacement of Cl^- with SO₄^2- converted the time courses of both K⁺ and Na⁺ diffusion potentials to a sustained type. These suggest that the pathway has a specially high permeability to K⁺ and lower permeabilities to Na⁺ and Cl^-. Triaminopyrimidine and kinetin similarly blocked K⁺ movement during stop-flow of a K⁺-free solution. The low R_t, a unique property of the segment, could be ascribed to the leakiness of the paracellular pathway from the comparison of input resistances of cells and cell surface areas between this segment and the proximal tubule. Based on these findings and other reported data, a novel mechanism of K⁺ supply was proposed which assumed the presence of a local pool of a high K⁺ concentration in the paracellular pathway and secretory movement of K⁺ through intercellular junctional complexes.