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 a miloride (1 mg kg-1 body wt) to block tubular potassium secretion, and with bumetanide (30 mug kg-1 body 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 2 32 +/- 56, 520 +/- 59 and 958 +/- 112 mumol min-1, respectively, at co nstant glomerular filtration rate (GFR). On average, the molar ratio b etween the inhibitory effects on bicarbonate and chloride reabsorption were 1: 2.2-2.4. Reabsorption was calculated at GFR 100 ml min-1: (re absorption 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. Frac tional potassium reabsorption remained constant at 0.31 +/- 0.03. Admi nistration of acetazolamide (100 mg kg-1 body wt) in eight dogs at [K] p 8 mM reduced fractional reabsorption of bicarbonate, chloride and so dium as much as in previous studies on normokalaemic dogs. We conclude that acute elevation of [K]p inhibits NaHCO3 transport and passive pr oximal tubular NaCl reabsorption. This inhibition is not related to ch anges in potassium secretion and carbonic anhydrase activity, but may be secondary to depolarization of the basolateral membrane.