Hypoxic inhibition of TASK-1 (Kcnk3 or K₂P3.1), a tandem-pore-domain background K⁺ channel, provides a critical link between reduced O₂ levels and physiological responses in various cell types. Here, we examined the expression and O₂-sensitivity of TASK-1 in immortalised adrenomedullary chromaffin (MAH) cells. In physiological (asymmetrical) K⁺ solutions, 3 µM anandamide or 300 µM Zn²⁺ inhibited a strongly pH-sensitive current. Under symmetrical K⁺ conditions, the anandamide and Zn²⁺-sensitive K⁺ currents were voltage-independent. These data demonstrate the functional expression of TASK-1, and cellular expression of this channel was confirmed by RT-PCR and Western blotting. At concentrations which selectively inhibit TASK-1, anandamide and Zn²⁺ were without effect on the magnitude of the O₂-sensitive current or the hypoxic depolarisation. Thus, TASK-1 does not contribute to O₂ sensing in MAH cells, and demonstrates the failure of a known O₂-sensitive K⁺ channel to respond to hypoxia in an O₂-sensing cell type. These data demonstrate that ultimately the sensitivity of a particular K⁺ channel to hypoxia is determined by the cell, and we propose this is achieved by coupling distinct hypoxia signalling systems to individual channels. Importantly, these data also reiterate the indirect O₂-sensitivity of TASK-1, which appears to require the presence of an intracellular mediator.