Sodium-Independent Active Potassium Reabsorption in Proximal Tubule of the Dog

Abstract

A B S T R A C T Prior studies of proximal tubule reabsorption have failed to distinguish conclusively between a separate active K+ transport system and K+ movement linked to Na+ reabsorption. To attempt to dissociate movement of K+ from Na+ and Ca++, recollection micropuncture experiments were performed in proximal tubules of intact and thyroparathyroidectomized (TPTX) dogs under two different conditions known to inhibit Na+ reabsorption: saline expansion to 5% body wt, and 5 mg/kg acetazolamide. A control hydropenic group was also studied. Tubular concentrations of K+, Na+, and Ca++ were measured by electron probe analysis. During initial collections, mean±i-SEM tubular fluid/plasma (TF/P)K+ was 1.07 +0.05, 1.05+0.05, and 1.00+0.03 in intact hydropenic (n = 7), saline (s = 6), and acetazolamide (i = 8) groups; fractional reabsorption (FR) of K+ in proximal tubules was 0.35, 0.39, and 0.31 respectively. After saline, (TF/P)nui n fell from 1.81 to 1.34 (P <0.01); (TF/P) K+, (TF/P) Na+, and tubular fluid/ultrafiltrate, (TF/UF)c.++ did not change, so that FR of all three ions fell proportionately. After acetazolamide, however, despite a 24% inhibition of FR of Na+ and Ca++, (TF/P)K+ fell to 0.85±0.04 (P < 0.005) so that FR of K+ was unchanged at 0.34.In three corresponding groups of TPTX dogs, similar results were obtained. Acetazolamide (n = 7) inhibited FR of Na+ and Ca++ by 41%, but (TF/P)x+ fell from 1.03±0.03 to 0.89±0.04 (P <0.005) so that FR of K+ was unchanged (0.36-0.34). A separate uphill transport system for K+ in proximal tubules is therefore unmasked by acetazolamide, a drug which selectively inhibits Na+ (and Ca++) reabsorption. Saline, on the other hand, inhibits net reabsorption of all three ions, probably by increasing passive backflux via intercellular channels.

Effects of Acetazolamide on Proximal Tubule Cl, Na, and HCO3 Transport in Normal and Acidotic Dogs during Distal Blockade

“…Beck et al (51) have reported that ACZ did not change fractional reabsorption of K in the proximal tubule. In addition it is generally accepted that the bulk of urinary K is derived from a distal secretory process (40,52,53) and that K secretion is dependent upon urinary flow rate, per se (54)(55)(56).…”

Estimated potassium reflection coefficient in perfused proximal convoluted tubules of the anaesthetized rat in vivo.

“…secondary active transport. A K+-H+-ATPase has been demonstrated in distal portions of the nephron (see Wingo & Cain, 1993 for review) but as yet there has been no evidence of any active transport of K+ in the proximal tubule of rats although there has been a suggestion of active K+ reabsorption in dogs (Beck, Senesky & Goldberg, 1973).…”

Renal tubular control of potassium transport

“…Proximal tubular potassium concentrations are close to that of plasma potassium concentrations. Normally, the rate of reabsorption of potassium along the proximal convoluted tubule is tightly coupled to that of sodium and water, although after acetazolamide [14] and after unilateral nephrectomy [15] proximal tubular sodium reabsorption is depressed whereas that of potassium continues at a fairly undiminished rate. This demonstrates that, potentially at least, proximal tubular potassium transfer may be regulated independently of sodium and of fluid transport.…”

“…First, tubule fluid/plasma potassium concentration ratios may fall to values less than unity, and hence active transport must be involved in these tubule segments having a lumen negative potential. Secondly, administration of acetazolamide, known to inhibit hydrogen ion transport across the proximal tubule [14] and which as been shown to prevent both the increase in chloride concentration [51] as well as the development of lumen-positive potentials [50], does not inhibit potassium reabsorption and the establishment of luminal potassium/plasma concentration ratios of less than unity [14].…”