The chemosensing glomus cells of the rat carotid body express two O2-sensitive K+ channels, BKCa channels and a TASK-like leak K+ channel. Inhibition of these channels by hypoxia causes cell depolarization, voltage-gated Ca2+ influx and neurotransmitter release. Although the identity of the upstream O2 sensor is still controversial, that the activity of BKCa is regulated not only by O2 but also by the gaseous compounds CO and H2S, suggests that integration of these signals may be crucial to the physiological response of the tissue. Thus, the ability of BKCa to respond to lowered O2 is enhanced by its co-localization with hemeoxygenase-2, an enzyme which generates CO in the presence of O2. Since CO is a potent BKCa channel opener, its reduced concentration during O2 deprivation results is channel closure, thus conferring a degree of O2-sensitivity to the BKCa channel. Conversely, H2S is a potent BKCa channel inhibitor. H2S is produced endogenously by cystathionine-β-synthase and cystathionine-γ-lyase (both being expressed in rat carotid body), and its intracellular concentration is dependent upon the balance between its enzymatic generation and its mitochondrial breakdown. During hypoxia, mitochondrial oxidation of H2S in many tissues is reduced, leading to hypoxia-evoked rises in its concentration. This may be sufficient to inhibit BKCa channels are lead to carotid body excitation. Consequently, it appears possible that carotid body function may be heavily dependent upon regulated production/breakdown of two gases which have been classically thought of by their toxic properties, suggesting that the integration of signals from these newly emerging gasotransmitters may refine, or even define, responses of this tissue to hypoxia.