Fig. 4.

Effect of acetazolamide (ACZ) on HCO₃ ⁻ efflux in NBCe1 KO and WT intestinal mucosa. a–c Blocking the presumed alternative pathway for HCO₃ ⁻ production reduced the basal HCO₃ ⁻ output in all studied intestinal segments. While the inhibitory effect of ACZ was identical in NBCe1 KO and WT duodenum (a, n = 7), it was significantly stronger in WT jejunum (n = 7), indicating that carbonic anhydrases also augment NBCe1-mediated HCO₃ ⁻ supply (b). In cecal mucosa (n = ,6), the high rates of luminal alkalinisation dramatically decreased after ACZ application in the NBCe1 KO but not the WT, indicating complete compensation of carbonic anhydrase inhibition by NBCe1-mediated HCO₃ ⁻ uptake in the latter (and vice versa in the KO)