Effects of pressure on glucose transport in human erythrocytes.

The operation of the human red cell glucose transporter has been studied at normal and high hydrostatic pressure to identify the step(s) which involve a volume change. Pressure inhibited zero-trans and equilibrium exchange influx to similar extents, by decreasing the Vmax but not significantly changing the Km. The Bmax and Kd of specific [3H]cytochalasin B binding were unaffected by pressure indicating no change to the number or affinity of functional transporters at pressure. Passive glucose transport was inhibited by pressure in a manner consistent with permeation across the lipid bilayer. These data indicate that there is a major change in volume during the translocation step of the glucose transporter which is rate-limiting for transport.