Effect of luminal potassium on cellular sodium activity in the early distal tubule of Amphiuma kidney.

From previous studies it is known that a furosemide-sensitive sodium chloride cotransport system is operative in the luminal cell membrane of the early distal amphibian tubule. Since inhibition of sodium chloride cotransport prevents potassium reabsorption in this nephron segment, experiments were carried out to evaluate further the possible relationship between sodium chloride and potassium transport by studying the changes of cellular sodium activity following luminal deletion of potassium ions. Sodium-sensitive liquid ion exchange microelectrodes and conventional microelectrodes were employed to determine the transepithelial potential (PDte), the peritubular cell membrane potential (PDpt) and the intracellular sodium activity (Nai+) in the presence and absence of luminal potassium. The ratio of the luminal cell membrane resistance over the peritubular cell membrane resistance (Rlu/Rpt) was also estimated. When potassium ions are omitted from the luminal perfusate, PDpt hyperpolarizes by some 20 mV, PDte approaches zero and Nai+ decreases by about 40%. Rlu/Rpt is more than doubled in the presence of a potassium-free perfusate. Both potential and resistance changes are fully reversible. Similar results were obtained in experiments in which Barium ions (1 mmol/1 BaCl2) were present during the luminal potassium substitution. Our results indicate that absence of potassium inhibits luminal sodium chloride entry; as a result of continued peritubular sodium extrusion cellular sodium activity falls. The increase of Rlu/Rpt following perfusion with a potassium-free perfusate is interpreted as a decrease of a significant electrodiffusive potassium conductance in the luminal cell membrane.