Figure 5. CFTR-dependent HCO₃⁻ conductance at the apical membrane of permeabilized control and CFTR knock-down (CFTR-KD) Calu-3 monolayers.

The basolateral membrane was permeabilized using nystatin and an apical-to-basolateral HCO₃⁻ gradient 25 → 0 mmol l⁻¹ was imposed across the monolayer. A, forskolin (Fsk, 10 μmol l⁻¹) stimulated a large inward current of ∼8 μeq cm⁻² h⁻¹. Forskolin-stimulated inward current in control cells was abolished by the CFTR inhibitor CFTR_inh-172 (inh172). Forskolin and CFTR_inh-172 had little effect on CFTR-KD monolayers. B, summary of short-circuit currents measured across control (n= 2) and CFTR-KD (n= 3) cells in the presence of a bicarbonate gradient. Forskolin-stimulated secretion (ΔI_sc) was almost abolished in CFTR-KD cells. Means ± SEM, P < 0.01.