The direct effects of desoxycorticosterone on skeletal muscle electrolyte metabolism.

It has been found that the primary effects of DCA upon skeletal muscle, particularly the effect upon sodium movements, are masked by electrolyte shifts that are secondary to muscle potassium depletion. The muscle potassium depletion is caused by an action of DCA to promote potassium excretion via the kidney and digestive tract. When muscle potassium losses were prevented in an eviscerated preparation, a direct effect of DCA to decrease cellular sodium was demonstrated in this tissue for the first time. In addition, direct actions of this steroid to increase total muscle carbon dioxide and to cause an extracellular alkalosis were observed in experiments where no potassium losses occurred. Calculations of intracellular pH based derived from carbon dioxide measurements reveal that control animals had a muscle pH in the vicinity of 7. DCA treatment of both intact and eviscerated animal caused the muscle cell to become alkalotic. These experiments indicated that DCA exerts and effect upon muscle acid-base balance in the absence of any changes in muscle potassium. Amino acid studies failed to support the observations of other workers that basic amino acids, particularly lysine, are mobile cations in muscle cells sufficient to counteract metallic cation deficiencies was detected. No reproducible changes in basic amino acids were observed following acid-based changes in the muscle. Investigations of the barium-soluble fraction of muscle showed that the fraction is highly variable in size, and that it is not a protein suspension of barium carbonate.