Influence of acute potassium loading on renal phosphate transport in the rat kidney.

UNLABELLED: This study examined 1) whether potassium-induced depression of phosphate excretion is a parathyroid hormone-dependent phenomenon, and 2) whether such stimulation of tubular phosphate reabsorption capacity involves increased phosphate reabsorption in the distal tubule. Potassium was infused into intact rats (25 mumol X min-1 X kg-1) during stepwise addition of phosphate to the infusion and led to a significant drop in phosphate excretion; this effect was abolished in thyroparathyroidectomized (TPTX) animals. In intact rats the maximal tubular Pi reabsorption per milliliter of glomerular filtrate (max TRPi/ml GF) was significantly higher in the potassium group (2.54 +/- 0.06 mumol/ml GF) compared with the control group (2.31 +/- 0.06 mumol/ml GF) (means +/- SE). In TPTX rats no difference in max TRPi/ml GF was observed: 3.44 +/- 0.07 and 3.49 +/- 0.07 mumol/ml GF during potassium and sodium infusion, respectively. Free-flow micropuncture was carried out on superficial distal tubules of intact rats and fluid samples were analyzed for [3H]inulin and phosphorus (electron microprobe). Phosphorus delivery into the distal tubule was similar in control and potassium-loaded rats. Whereas net phosphorus reabsorption along the distal tubule was absent in the control group, intravenous potassium administration stimulated distal phosphorus reabsorption.
CONCLUSION: potassium stimulates renal phosphate reabsorption capacity, an effect that is abolished after TPTX. The potassium effect on phosphate occurs along the distal tubule.