Rats were made K deficient by diet, by the injection of desoxycorticosterone acetate, and by protein repletion of protein depleted rats fed K-free diets. The tissues were examined for increases in basic amino acids. Increased amounts of l (+) lysine, identified by chromatographic, electrophoretic, enzymatic and microbiological techniques have been found in the muscle and kidney of K-deficient animals. The lysine and/or the basic amino acid content as well as the Na, K and Cl content of muscle and plasma has been measured. Lysine contributes significantly to the total cations of muscle in K deficiency. On partial K repletion, some of this lysine is apparently completely oxidized.

No abstract

The acid-base balance of muscle from control and K-deficient rats was studied. From the measured buffering capacity, 8–11 mEq excess of anions or deficit of cations would be required to acidify 100 gm fat-free dry weight of muscle, 0.5 pH units. No evidence of increased organic acids, increased anionic equivalence of muscle proteins, or of decreased concentrations of weak bases which are potential cations in cell acidosis was found. This evidence, supplemented with data in the literature, fails to account for the cell acidosis reported in the literature. Reliability of the ‘chloride space’ as a measure of the extracellular phase of muscle in K deficiency has been confirmed by showing its agreement with the ‘raffinose space.’ The cell pH has then been calculated from the distribution of CO2 in muscle (indirect method) and from the pH of muscle homogenates (direct method) in control and K-deficient animals. Control and K-deficient muscle pH's are, respectively, 6.89 and 6.83 by the direct method, and 7.11 and 7.05 by the indirect method.