Epithelial Na⁺ absorption depends upon K⁺ channel activity (Gordon & MacKnight, 1991) and Ba²⁺ thus inhibits Na⁺ absorption in human airway epithelia. Whilst the target K⁺ channel has not been identified, there is evidence for K_Ca3.1 involvement (Gao et al. 2001; Clunes et al. 2005; McNeill et al. 2005), and so we cloned this channel from H441 cells, expressed it in CHO cells and studied its properties by recording currents from single cells held under voltage clamp. When [Ca²⁺]_i was buffered (5 mM EGTA) at 0.5 µM, K_Ca3.1 expression was associated with large, clotrimazole-sensitive (10 µM) currents (Fig. 1A) that reversed at a potential close to E_K (Fig. 1B). Increasing [K⁺]_o (Na⁺ replacement) depolarised these cells in the manner predicted for a selective K⁺ conductance (Fig. 1C) and so, under these conditions, the electrical properties of transfected cells are dominated by a selective K⁺ conductance. However, K_Ca3.1 expression had no overt effect upon membrane conductance when [Ca²⁺]_i was 0.2 µM, although EBIO (1 mM) increased conductance under these conditions but had no effect upon the currents recorded at 0.5 µM [Ca²⁺]_i (Fig. 1D). This is consistent with the view that EBIO sensitizes K_Ca3.1 to Ca²⁺ (Pedersen et al. 1999). K_Ca3.1 thus appears inactive when [Ca²⁺]_i is ~0.2 µM suggesting that this channel does not contribute to resting K⁺ conductance (G_K). Indeed, patch clamp studies of H441 cells, undertaken in the presence of amiloride (10 µM, included to block G_Na), showed (n = 6) that 10 µM clotrimazole had no effect upon V_m in unstimulated cells (control: 47.5 ± 6.7 mV, clotrimazole: 48.0 ± 6.8 mV) despite a clear, K⁺-evoked depolarization (control: 52.8 ± 6.8 mV, 113 mM K⁺: 25.7 ± 4.0, P < 0.001, Student’s paired t test). K_Ca3.1 expression thus appears to confer a latent K⁺ conductance upon the membrane that is activated by increased [Ca²⁺]_i or EBIO. However, since these channels do not contribute to resting G_K, they cannot be involved in basal Na⁺ absorption.