Effect of K depletion on renal K and Rb excretion: evidence for activation of K reabsorption.

Prolonged potassium depletion activates tubular transport mechanisms mediating potassium absorption. To study ion specificity and factors that modulate the activity of potassium transport pathways, fractional potassium excretion (FEK) was compared with that of rubidium (FERb) in control and potassium-depleted rats subjected to various experimental maneuvers. In control rats FEK considerably surpassed FERb (FEK/FERb 1.54 +/- 0.08; mean +/- SEM), whereas in potassium-depleted rats FEK was significantly lower than FERb (FEK/FERb 0.72 +/- 0.05). Preferential retention of potassium compared to rubidium in potassium-depleted rats was accentuated (FEK/FERb 0.33 +/- 0.01) when residual potassium secretion was inhibited by amiloride and K-H exchange stimulated by increased distal buffer delivery (metabolic alkalosis). When distal fluid and buffer delivery were increased in control animals by acetazolamide, FEK and FERb rose in parallel. In potassium-depleted rats only FERb but not FEK was enhanced by acetazolamide. These data demonstrate that both potassium secretory and potassium absorptive transport pathways prefer potassium to its congener rubidium. Prolonged potassium depletion activates a potassium absorptive mechanism which is stimulated by increased distal buffer delivery and which transports potassium more effectively than rubidium.