In this review, we have highlighted the roles of ion channels in carotid body chemotransmission of acute hypoxia. With the application of new technologies, significant breakthroughs have been made in the last decade. The discovery of oxygen-sensitive K(+) channels in rabbit glomus cells has generated the membrane model of hypoxic chemotransmission: the inhibition of oxygen-sensitive K(+) channels by hypoxia initiates the depolarization of glomus cells and increases the firing frequency of glomus cells. The depolarization of glomus cells activates voltage-gated Ca(2+) channels, elevating intracellular Ca(2+) which triggers the release of neurotransmitters. The correlation of these events in rabbit glomus cells has been shown. However, a large corpus of data indicates that various mechanisms may be involved in different species. In rats, Ca(2+)-activated K(+) channels are inhibited by hypoxia. The role of this inhibition on rat glomus cell function is controversial, and the contribution of leak-type K(+) channels to rat glomus cell depolarization has recently been proposed. On the other hand, in cats, nicotinic ACh receptors (ligand-gated cation channels) may play a key role in initiating the depolarization of glomus cells and increasing the cytosolic Ca(2+) of glomus cells in response to hypoxia. Hypoxic inhibition of oxygen-sensitive K(+) channels would participate to further depolarize cat glomus cells. Additionally, the activity of Cl(-) channels and the modulation of ion channels by neurotransmitters may influence the excitability of glomus cells. For generating action potentials in chemoreceptor afferent nerves, nicotinic ACh receptors appear to be involved in cats and rats.