The type-1 cell of the carotid body is a chemoreceptor which detects blood oxygen, pH and CO₂ levels. In response to hypoxia or hypercapnic acidosis these cells undergo membrane depolarisation followed by the initiation of electrical activity, voltage gated calcium entry and neurosecretion. The initial depolarisation in response to both hypoxic and acidic stimuli appears to be mediated primarily through the inhibition of a resting background K⁺ conductance. The channels responsible for this acid and oxygen sensitive K⁺ current display many of the characteristics of tandem-p-domain K⁺ channels and the TASK subgroup in particular. Specifically, the type-1 cell background K⁺ channels are relatively voltage insensitive and resistant to block by the classical K⁺ channel inhibitors TEA and 4-AP. They are, however, inhibited by acidosis, quinine, barium, external divalent cations (Mg²⁺, and Zn²⁺) and are activated by halothane (but not chloroform). We have recently observed that the background K⁺-channels of type-1 cells are also strongly inhibited by mitochondrial uncouplers, blockers of electron transport and blockers of ATP synthase. As in the case of hypoxia, this leads to rapid membrane depolarisation and calcium entry. Inhibitors of mitochondrial ATP synthesis have long been known to be very potent chemo-stimulants but it had been thought that their excitatory effects were due to calcium release from mitochondrial (and or other intracellular stores) rather than through changes in cell excitability. Inhibition of mitochondrial respiration was also observed to result in a loss of background K⁺ channel responsiveness to oxygen. These results suggest a fundamental link between cell energy status oxygen levels and the regulation of background K⁺ channel activity. Recent studies in excised inside out patches have further revealed that these TASK-like background K⁺ channels are strongly activated (up to 8-fold) by cytosolic ATP with a K_1/2 of approximately 2.3 mM. Changes in cytosolic ATP may therefore play an important role in the modulation of the activity of these channels both in response to changes in metabolism and oxygen.