M. Bailey et al., The relationship between distal tubular proton secretion and dietary potassium depletion: evidence for up-regulation of H+-ATPase, NEPH DIAL T, 14(6), 1999, pp. 1435-1440
Background. Dietary potassium depletion is associated with elevated plasma
bicarbonate concentration and enhanced bicarbonate reabsorption in the dist
al tubule. The relationship between distal proton secretion and potassium s
tatus was investigated by in vivo micro-perfusion of the superficial distal
tubule.
Methods, Experiments were performed on anaesthetized rats that had been mai
ntained on either a low-potassium or control diet for 3-5 weeks prior to ex
perimentation. The distal tubules were perfused at 10 nl/min with either a
standard or a barium chloride-containing solution, and the late distal tubu
lar transepithelial potential difference (V-te) and pH of the luminal fluid
were recorded using a double-barrelled voltage and ion-sensitive microelec
trode.
Results. In control rats, the V-te was -40.7 +/- 2.4 mV and the tubular flu
id pH was 6.44 +/- 0.07;in potassium-depleted animals, the V-te was -15.0 /- 1.4 mV and the pH was 6.76 +/- 0.03. The pH values in both groups of ani
mals were significantly lower than would be predicted from the V-te and sys
temic pH for passive H+ distribution, indicating active proton secretion. M
oreover, in hypokalaemic rats, this difference from predicted pH was signif
icantly greater than in control animals (control = 0.27 +/- 0.06 vs low-pot
assium = 0.46 +/- 0.03; P < 0.01), suggesting enhanced active proton secret
ion. During perfusion with a solution containing BaCl2, the late distal tub
ule V-te became lumen positive in potassium-depleted rats, contrasting with
an increased lumen negativity in potassium-replete controls. The barium-in
duced lumen-positive potential difference observed in the hypokalaemic rats
was abolished by intravenous administration of acetazolamide.
Conclusion. These data are consistent with enhanced electrogenic proton sec
retion (H+-ATPase) during dietary potassium deprivation.