Background: Previous studies suggest that sodium, potassium-adenosinetriphosphatase (Na+, K(+)-ATPase) activity in skeletal muscle is increased during sepsis, but the molecular mechanisms are not well understood. We tested the hypothesis that increased muscle Na+,K(+)-ATPase activity during sepsis is associated with increased expression of messenger RNA for the Na+,K(+)-ATPase alpha-1, alpha-2, and beta-1 subunits and increased amounts of the enzyme protein.
Study design: Extensor digitorum longus muscles were harvested from rats 16 hours after induction of sepsis by cecal ligation and puncture or sham operation. The Na+,K(+)-ATPase activity was determined spectrophotometrically. Messenger RNA levels for the alpha-1, alpha-2, and beta-1 subunits of Na+,K(+)-ATPase were determined by Northern blot analysis. Enzyme protein levels were measured by Western blot analysis and tritium-ouabain binding assay.
Results: Muscle Na+,K(+)-ATPase activity was 46 percent higher in rats that had sepsis than in rats that underwent sham operation (p < .05). No significant differences between septic and control groups were noted in messenger RNA levels for the Na+,K(+)-ATPase subunits. Western blot analysis and tritium-ouabain binding revealed no difference in enzyme protein expression between septic and control animals.
Conclusions: Results suggest that sepsis increases skeletal muscle Na+,K(+)-ATPase activity without affecting enzyme messenger RNA or protein levels. The results are consistent with an increased catalytic constant for individual Na+,K(+)-ATPase protein units, an atypical mechanism for this enzyme.