Renal acidification in renal proximal tubule is thought to be mediated by luminal Na-H antiporter and the HCO3- generated by this antiporter is removed from the cell by a basolateral Na-HCO3 cotransporter. To study the effect of respiratory acid-base disorders on these transport systems, we have measured the Na-HCO3 cotransport in basolateral membranes and Na-H antiporter in luminal membranes in control rabbits, rabbits exposed to 10% CO2 (chronic hypercapnia), and rabbits exposed to 10% O2-90% N2 (chronic hypocapnia). The Vmax of HCO3(-)-dependent 22Na uptake was significantly higher in chronic hypercapnia than controls (2.54 +/- 0.03 vs. 1.18 +/- 0.21 nmol.mg protein-1.3 s-1, P less than 0.001). Likewise, the Vmax of the Na-H antiporter was also increased compared with controls (924.9 +/- 42.1 vs. 549.1 +/- 62.8 fluorescence units (FU).300 micrograms protein-1.min-1). In chronic hypocapnia, the Vmax of Na-HCO3 cotransport was lower than controls (0.72 +/- 0.11 vs. 1.18 +/- 0.21 nmol.mg protein-1.3 s-1, P less than 0.05). There was no difference, however, in the Vmax of the Na-H antiporter between hypocapnia and control (524.2 +/- 24.3 vs. 549.1 +/- 62.8, FU.300 micrograms protein-1.min-1). The Vmaxs of the Na-HCO3 cotransport and of the Na-H antiporter in hypocapnic, control, and hypercapnic rabbits were linearly related (r = 0.81), suggesting a simultaneous adaptation of the two systems in respiratory acid-base disorders.(ABSTRACT TRUNCATED AT 250 WORDS)