We have investigated A-type K⁺ currents in pulmonary neuroepithelial bodies (NEB) using neonatal rabbit lung slice preparation. The whole-cell K⁺ current was slowly inactivating with activation threshold of ~ -30 mV and was blocked ~ 27% by BDS-I (3 µM), a selective blocker of Kv3.4 subunit, and reduced ~ 20% by TEA (100µM). The BDS-I- sensitive component had an average peak value of 189 ± 14 pA, and fast inactivation kinetics that could be fitted by one-component exponential function with a time constant of (1 ) 77 ± 10 ms. This Kv slowly inactivating current was also blocked by HpTx-2 (0.2 µM), a blocker of Kv4 subunit with an average peak value of 234 ± 23 pA and a time constant of ( ) 82 ± 11 ms. Hypoxia (PO₂ = 15 - 20 mmHg) inhibited the slowly inactivating K⁺ current by ~ 47 %, during voltage steps from -30 to + 30 mV, and no further inhibition occurred when TEA was combined with hypoxia. Nicotine (50 µM and 100 µM) suppressed the slowly inactivating K⁺ current by ~24% and ~40%, respectively and was not reversed by mecamylamine. In situ hybridization and double-label immunofluorescence detected expression of mRNA's and respective channel proteins for Kv3.4 and Kv4.3 subunits in NEB cells. We conclude that the hypoxia - sensitive current in NEB cells is carried by slowly inactivating A-type K⁺ channels, and that exposure to nicotine may directly affect their function.