Plasma potassium concentration as a determinant of proximal tubular NaCl and NaHCO₃ reabsorption in dog kidneys

To examine whether an acute increase in plasma potassium concentration ([K]_p) may inhibit proximal tubular transport, clearance studies were performed in seven anaesthetized, volume expanded dogs treated with amiloride (1 mg kg^-1body wt) to block tubular potassium secretion, and with bumetanide (30 μg kg^-1body wt) to inhibit NaCl reabsorption in Henle's loop. As [K]_p was raised in steps from 2.6 ± 0.2 to 7.9 ± 0.2 mm, bicarbonate, chloride, and sodium reabsorption decreased by 232 ± 56, 520 ± 59 and 958 ± 112 μmol min^-1, respectively, at constant glomerular filtration rate (GFR). On average, the molar ratio between the inhibitory effects on bicarbonate and chloride reabsorption were 1:2.2–2.4. Reabsorption was calculated at GFR 100 ml min^-1: (reabsorption 100/GFR (mmol min^-1). It was inversely correlated to In [K]_p with r=–0.82 for bicarbonate and with r =–0.89 for chloride. Fractional potassium reabsorption remained constant at 0.31 ± 0.03. Administration of acetazolamide (100 mg kg^-1body wt) in eight dogs at [K]_p 8 mm reduced fractional reabsorption of bicarbonate, chloride and sodium as much as in previous studies on normokalaemic dogs. We conclude that acute elevation of [K]_p inhibits NaHCO₃ transport and passive proximal tubular NaCl reabsorption. This inhibition is not related to changes in potassium secretion and carbonic anhydrase activity, but may be secondary to depolarization of the basolateral membrane.