The OMCDi absorbs HCO3- at high rates but it is not clear how it responds to metabolic acidosis. We measured net HCO3- transport in isolated perfused OMCDi taken from control and acidotic(NH4Cl fed × 3 d) rabbits. Tubules from acidotic rabbits showed higher rates of HCO3- absorption (17.1 ± 0.3 vs. 12.9± 0.2 pmol/min/mm, p < 0.01). There was no difference in the 10μM SCH28080-sensitive flux (H+,K+-ATPase; 5.9 ± 0.1 vs. 5.8 ± 0.2 pmol/min/mm), whereas there was a higher 5-10 nM bafilomycin-sensitive HCO3- absorptive flux (H+-ATPase; 11.3 ± 0.3 vs. 7.0 ± 0.2 pmol/min/mm, p<0.01). Transport was then measured in other OMCDi segments before and after incubation for 1 h at pH 6.8 followed by 2 h at pH 7.4 (in vitro acidosis). Acid incubation in vitro stimulated HCO3- absorption (12.5 ± 0.4 to 16.8 ± 0.4 pmol/min/mm; p < 0.05). while incubation at pH 7.4 for 3 h did not change basal rate (12.5 to 12.4 pmol/min/mm). The H+,K+-ATPase sensitive flux did not change after acid incubation (5.4 ± 0.4 to 6.1± 0.2 pmol/min/mm), while there was a 60% increase in H+-ATPase sensitive flux (6.6 ± 0.3 to 10.8 ± 0.3 pmol/min/mm). In 2 segments obtained from acidotic animals and incubated at low pH there was a higher basal rate and a further increase in HCO3- absorption(17.1 to 21.4 pmol/min/mm).

These data indicate that HCO3- absorption (H+ secretion) is stimulated by metabolic acidosis in the OMCDi, primarily by an increase in H+-ATPase activity. This adaptation helps the animal to maintain homeostasis during metabolic acidosis.