The cystic fibrosis transmembrane conductance regulator (CFTR) is a cAMP/protein kinase A regulated chloride (Cl^–) channel localised to the apical membrane of epithelial cells. It plays an important role in maintaining salt and fluid balance in these cells. As well as an ion channel CFTR has been found to regulate a number of transport proteins, e.g. the epithelial sodium channel ENaC. In cystic fibrosis (CF) which is caused by mutations in CFTR there is abnormal calcium (Ca²⁺) homeostasis in airway epithelial cells. Given the role CFTR plays as a channel regulator, cation currents in normal and CF airway epithelial cells were examined. Whole cell ruthenium red (RR, 100 μM) and cadmium (Cd²⁺, 100 μM) sensitive conductances were measured in 16HBE14o- and CFBE41o- cells under control conditions or after cAMP stimulation. The bath solution contained NaCl and the pipette solution contained CsAsp. A ramp protocol measured currents between +60 to -100mV. Statistical significance was tested using Students t-test and assumed at the 5% level. Under control conditions both 16HBE14o- and CFBE41o- cells possessed a RR and Cd²⁺– sensitive conductance. Cd²⁺ caused a significant reduction in the size of the RR-sensitive conductance compared to RR on its own in 16HBE14o- cells (397.8 ± 77.9µS/cm², n=8 vs 881 ± 187.6µS/cm², n=9 respectively) but not in CFBE41o- cells (414.4 ± 74.7µS/cm², n=10 vs 460.9 ± 112.4µS/cm²⁺, n=7 respectively). Under cAMP stimulated conditions both 16HBE14o- and CFBE41o- cells possessed a RR-sensitive conductance. After cAMP stimulation 16HBE14o- cells failed to show a Cd²⁺– sensitive conductance, while CFBE41o- cells possessed a small Cd²⁺-sensitive conductance (184.1 ± 38.5µS/cm², n=9). In stimulated 16HBE14o- and CFBE41o- cells Cd²⁺ had no effect on the size of the RR-sensitive conductance compared to RR on its own (428.5 ± 47.8µS/cm², n=13 vs 542.5 ± 132.8µS/cm², n=11 in 16HBE14o- cells and 613.2 ± 143.3µS/cm², n=12 vs 567.4 ± 112.3µS/cm², n=13 in CFBE41o- cells). Consistent with previously found selectivity differences, these data suggest that different cation channels are found in normal and CF airway epithelial cells. Further studies are needed to confirm whether these differences are a consequence of mutations in CFTR.