Luminal buffer transport in rat cortical tubule: relationship to potassium metabolism.

Abstract

Free-flow micropuncture studies were performed on superficial rat tubules and titratable acid (TA), sodium and potassium concentrations, and tubular pH were measured in control, acutely K-loaded, and chronically K-depleted animals. The proximal tubule is a key site of TA formation. Under control conditions, significant amounts of TA were lost along the loop of Henle. TA delivery (in pmol X min-1) to the late proximal tubule (LP) was 23.66 +/- 2.38 (mean +/- SE), that to the early distal tubule (ED) was 17.24 +/- 1.73, and little further loss occurred along more distally located nephron sites. In acute hyperkalemia, urinary TA excretion (in mumol X min-1) was lower than under control conditions (0.56 +/- 0.04 vs. 1.01 +/- 0.07); TA delivery to the LP (18.50 +/- 1.93) was slightly reduced compared with the controls (a change not reaching statistical significance). TA delivery to the ED was also reduced (11.54 +/- 1.04); significant amounts of TA were lost along the loop of Henle and a significant further loss occurred along the distal tubule since TA delivery to the late distal tubule (LD) was only 7.41 +/- 0.83. As luminal pH along both proximal and distal tubules in K-loaded rats was indistinguishable from that of control rats, a major factor responsible for decreased distal TA formation in K-loaded animals was diminished buffer delivery. In chronic potassium depletion urinary TA excretion was also lowered (0.30 +/- 0.06); only a moderate part of this effect was due to increased pH along the nephron. Increased buffer reabsorption along the proximal tubule (TA delivery to LP was 14.32 +/- 2.01) contributed mainly to the reduced rate of titratable acid excretion.