Selective dietary potassium depletion and acid-base equilibrium in the rat

1. K⁺ depletion of two kinds was induced in two groups of rats by selective dietary restriction for up to 5 weeks. Complete metabolic studies for H⁺, K⁺, Na⁺ and Cl⁻ were carried out daily during weeks 1, 3 and 5.

2. In control rats of group A (receiving K⁺ with sodium chloride), plasma pH (7.47) and HCO⁻₃(25 mmol/l), as well TA (titratable acid) —- HCO⁻₃ and NH⁺₄ urinary excretion rates, were stable, while balances were nil for K⁺ and slightly positive for Cl⁻. In K⁺-deprived rats of group A receiving sodium chloride, a progressive metabolic alkalosis developed (plasma pH reached 7.57 and HCO⁻₃ 35.8 mmol/l by 5 weeks), and TA - HCO⁻₃ and NH⁺₄ urinary excretion rates were not different from controls. Plasma K⁺ fell progressively from 4.20 to 2.20 mmol/l, with negative K⁺ balance. Balances for Na⁺ and H₂O were highly positive and plasma renin activity and aldosterone decreased by week 5. Hypochloraemia developed with positive Cl⁻ balance.

3. In control rats of group B (receiving K⁺ with neutral sodium phosphate), a slight metabolic alkalosis developed, and TA - HCO⁻₃ excretion rate was increased compared with control rats of group A. Balances were slightly negative for K⁺ and Cl⁻. In K⁺-deprived rats of group B receiving neutral sodium phosphate, a profound metabolic alkalosis developed (plasma pH reached 7.60 and HCO⁻₃ 42.6 mmol/l by 5 weeks), and TA-HCO⁻₃ and NH⁺₄ excretion rates were at no time different from those of control rats of group B. Plasma K⁺ fell progressively from 4.25 to 2.30 mmol/l, and K⁺ balance was more negative than that in control rats of group B. Hypochloraemia developed with a negative Cl⁻ balance.

4. In both K⁺-restricted groups, a linear negative correlation was observed between plasma HCO⁻₃ (or pH) and plasma K⁺. These results suggest that metabolic alkalosis does occur in sustained selective K⁺-depletion in rats. Metabolic alkalosis could be generated essentially by net transfer of H⁺ from extracellular fluid (ECF) into cells, probably in exchange for K⁺ in the reverse direction. Metabolic alkalosis could be maintained by an increase in tubular reabsorption of filtered HCO⁻₃, probably via an enhanced Na⁺/H⁺ exchange in the proximal tubule in sodium chloride-loaded rats, which may account for the ECF volume expansion with low plasma renin activity and aldosterone, and via an enhanced Cl⁻/HCO⁻₃ exchange in distal nephron in sodium phosphate-loaded rats.