Oxygen sensitive Kv channels in the carotid body

Hypoxic inhibition of K+ channels has been documented in many native chemoreceptor cells, and is crucial to initiate reflexes directed to improve tissue O2 supply. In the carotid body (CB) chemoreceptors, there is a general consensus regarding the facts that a decrease in PO2PO2 leads to membrane depolarization, increase of Ca2+ entry trough voltage-dependent Ca2+ channels and Ca2+-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+ ((KO2)(KO2)) channels in the CB is hotly debated. Clearly there are inter-species differences, and even in the same preparation more that one KO2KO2 may be present. Here we recapitulate our present knowledge of the role of voltage dependent K+ channels as KO2KO2 in the CB from different species, and their functional contribution to cell excitability in response to acute and chronic exposure to hypoxia.