Abstract
Summary
Intracellular bicarbonate content ([HCO3 -] i ) of rat skeletal muscle was derived from CO2 distribution in animals subjected to CO2 inhalation and K deficiency applied singly and together. The objectives were to determine (i) whether or not [HCO3 -] i would be reduced in acidotic, low-K muscle, and (ii) whether the [HCO3 -] i increase due to CO2 inhalation would be the same in normal and K-deficient animals. There was a 20% reduction in the CO2-derived [HCO3 -] i of low-K muscle. A 20% reduction was also obtained when deriving [HCO3 -] i from DMO pH i . The [HCO3 -] i increment due to CO2 inhalation was sufficiently less in low-K muscle to yield, upon analysis of variance, a statistical interaction between the two stresses applied. This interaction was indicative of less buffering by low-K muscle. The data strongly suggest that the acidotic, low-K cell is defending against H+ whose origin is metabolic.
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