The role of potassium in the prevention of alkalosis

• 1.1. Loads of sodium bicarbonate were administered to normal rats in drinking water along with known amounts of potassium and chloride. Alkalosis did not develop after two weeks as long as potassium chloride intake exceeded 0.5 mM/kg./day even though sodium bicarbonate intake amounted to 10 to 30 mM/ kg./day. It was not possible to produce alkalosis in this way in the absence of potassium deficiency, as demonstrated by muscle analysis.
• 2.2. Sodium bicarbonate, 15 mM per kg., was injected into normal and potassium-deficient rats, and urine was collected for the subsequent twelve hours. Serum and muscle analyses were obtained at the end of that time also. Normal animals excreted 10 mEq. of sodium and 5 mEq. of potassium per kg. of body weight in the twelve-hour period following loading. Essentially no chloride was excreted and alkalosis was not present after twelve hours. Potassiumdeficient animals excreted only 6 mEq. of sodium per kg. and no potassium. Almost 1 mEq. of chloride per kg. of body weight was excreted by the potassium-deficient animals and severe hypochloremic alkalosis was present twelve hours after loading.
• 3.3. Potassium bicarbonate, 3 mM per kg., was injected twice a day into potassium-deficient rats with hypochloremic alkalosis. No sodium or chloride was administered. After 24 mM per kg. of potassium bicarbonate had been administered, serum bicarbonate concentration fell to normal and serum chloride concentration rose to normal. This correction was associated with relatively little increase in bicarbonate excretion and with essentially no change in urinary pH or titratable acidity. Cation was excreted with organic anion, a large part of which was shown to be citrate.These results suggest that citrate may be substituted for chloride in the renal defense against alkalosis so that sodium is excreted without chloride and without change in urinary pH. Potassium would seem to be essential for the maximal conservation of chloride in this way.
• 4.4. These findings suggest that potassium deficiency may alter the ratio in which sodium and chloride are reabsorbed from glomerular filtrate. Such an alteration leads to changes not only in extracellular concentrations but also in extracellular volume.