Mechanisms of sodium, potassium and chloride transport by the renal distal tubule.

The distal tubule contributes importantly to renal sodium and chloride reabsorption and potassium secretion. Changes in various factors acting from the luminal or basolateral side of the distal tubule can alter rates of net ion transport. Experiments were designed to examine some of the factors of luminal fluid that can alter sodium, chloride and potassium transport rates. This was accomplished by employing in vivo microperfusion techniques to change luminal sodium, potassium and chloride concentrations and fluid flow rate independent of any effects on systemic homeostatic mechanisms. Results of these experiments indicate that increasing the rate of fluid flow in the distal tubule, within the physiologic range, stimulates potassium secretion, even when sodium concentration does not change. Low sodium concentrations inhibit net potassium secretion only when they are below those that have been measured in this segment under physiologic conditions. Potassium secretion rates increase significantly when the luminal chloride concentration is reduced, an effect that can be dissociated from changes in transepithelial voltage. Sodium absorption is limited by low luminal chloride concentration and chloride absorption is limited by low luminal sodium concentration. These results and others have led us to postulate that at least four different pathways mediate Na, K and Cl transport across the luminal membrane of distal tubule cells. Two pathways permit diffusive movement of cations, one an amiloride inhibitable channel for sodium, the other a barium inhibitable channel for potassium. Two other pathways appear to mediate coupled K-Cl secretion and Na-Cl absorption across the apical membrane of distal tubule cells. A new model of apical membrane transport pathways in the distal tubule is presented.