Effect of hydrostatic pressure on ion transport and metabolism in human erythrocytes

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Abstract
Influence of pressure on active and passive Na transport and K transport was studied in the human erythrocyte. Both active and passive transport was reversibly inhibited approximately 40% by pressures in the range of 30-150 ATA [atmosphere absolute pressure]. Half-maximal inhibition was found at .apprx. 20 ATA. The inhibition of transport by pressure was dependent on intracellular Na concentration. Pressure had no effect if the cell Na was above 25 or below 2 meq/l cells. Total, Mg2+-ATPase and Na+-K+-ATPase activities were evaluated in erythrocyte membranes over a pressure range from 1-136 ATA. Both total and Mg2+-ATPase showed a biphasic response to pressure, first increasing and then decreasing in activity. Na+-K+-ATPase displayed a monotonic activation by pressure up to 136 ATA. Red cell glycolytic intermediates, metabolites and metabolite ratios were examined after incubation at pressures from 1 to 150 ATA. ATP and ATP/ADP increased at every pressure; ADP declined at every pressure. Glcuose utilization was not influenced by pressure. Small declines in pyruvate and lactate were observed at some pressures. NAD+/NADH computed from pyruvate/lactate ([NAD+]/[NADH] = [H+]/K1 .times. [pyruvate]/[lactate]) changed little, indicating that pressure does not introduce any additional rate-limiting steps in glycolysis, since these enzyme cofactors exist in rate-limiting concentrations and are therefore sensitive to changes in overall cell metabolism.