Hypoxic inhibition of K(+) channels has been documented in many native chemoreceptor cells, and is crucial to initiate reflexes directed to improve tissue O(2) supply. In the carotid body (CB) chemoreceptors, there is a general consensus regarding the facts that a decrease in P(O2) leads to membrane depolarization, increase of Ca(2+) entry trough voltage-dependent Ca(2+) channels and Ca(2+)-dependent release of neurotransmitters. Central to this pathway is the modulation by hypoxia of K(+) channels that triggers depolarization. However, the details of this process are still controversial, and even the molecular nature of these oxygen-sensitive K(+) (K(O2)) channels in the CB is hotly debated. Clearly there are inter-species differences, and even in the same preparation more that one K(O2) may be present. Here we recapitulate our present knowledge of the role of voltage dependent K(+) channels as K(O2) in the CB from different species, and their functional contribution to cell excitability in response to acute and chronic exposure to hypoxia.