Potassium excreted by the kidney is derived largely from potassium secretion by the distal tubule and collecting duct. It is this secreted fraction that responds to systemic changes and is mainly responsible for regulation of potassium balance. A smaller fraction of the excreted quantity comes from potassium that is filtered and escapes reabsorption. Variations in the rate of reabsorption may alter potassium secretion under some circumstances. In the proximal tubule, reabsorption of potassium appears to involve interaction with a membrane mechanism. The contribution of descending limb potassium secretion to final potassium secretion is a present uncertain because of the inaccessibility of inner cortical distal tubules and collecting ducts in intact animals. Changes in plasma K, plasma aldosterone, and plasma acidity all appear to affect distal potassium secretion by influencing the uptake of potassium from blood to cell and thus raising the intracellular potassium. Changes in extracellular fluid volume, which increase urine flow and sodium excretion, appear to increase distal potassium secretion as a consequence of increases in the flow rate of luminal fluid. Flow-dependent changes in luminal potassium concentration may be involved but they do not appear to act by simply increasing the passive electrochemical driving force (assessed across the entire epithelium). Our understanding of the cellular mechanisms controlling renal potassium secretion is becoming clearer as it becomes possible to identify and to separate for a study a potentially confusing array of interacting variables.