We have examined the activity and kinetic characteristics of the Na+-H+ exchanger in renal cortical brush-border membrane vesicles (BBMV) prepared from rabbits adapted to chronic hypocapnia in order to address whether this transporter might contribute to the suppressed proximal bicarbonate reabsorption characteristic of this disorder. Chronic hypocapnia was induced by exposing animals to 9% O2 for a 5-day period. In comparison with paired, contemporaneous controls, an average delta PaCO2 of 13 mmHg and an average delta [HCO3-] of 7.3 meq/l were obtained. Chronic hypocapnia led to a significant suppression of the 22Na+ uptake by BBMV; at the 3-s mark, a 30% suppression was observed (chronic hypocapnia, 4.05 +/- 0.43 nmol/mg protein; control, 5.72 +/- 0.39 nmol/mg protein) (P less than 0.01). A significant decrease in the Vmax of the antiporter was noted (chronic hypocapnia, 622.7 +/- 86.8 nmol.mg protein-1.min-1; control 857.5 +/- 64.8 nmol.mg protein-1.min-1) (P less than 0.01), whereas the Km for sodium remained unaltered. The specificity of this adaptation was supported by showing that Na+-dependent uptake of D-[3H]glucose by BBMV was not significantly different between chronic hypocapnia and control. Chronic normocapnic hypoxemia left Na+-H+ exchange activity undisturbed. We conclude that the observed change in the BBMV Na+-H+ antiporter might be responsible, at least in part, for the suppressed renal bicarbonate reabsorption characteristic of chronic hypocapnia and that a consequence of the hypocapnic state itself mediates this adaptation.
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