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 HCO3(25 mmol/l), as well TA (titratable acid) —- HCO3 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 HCO3 35.8 mmol/l by 5 weeks), and TA - HCO3 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 - HCO3 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 HCO3 42.6 mmol/l by 5 weeks), and TA-HCO3 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 HCO3 (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 HCO3, 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/HCO3 exchange in distal nephron in sodium phosphate-loaded rats.

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