Carotid bodies (CB) are the major oxygen-sensing organs. They are responsible for the hyperventilation reflex occurring both in acute and chronic hypoxia (CH). The mechanisms of O₂-sensing and genesis of CB responses are not fully resolved, however, it is known that hypoxia depolarizes chemoreceptor cells via O₂-sensitive K⁺-channel inhibition, causing voltage-gated calcium influx and neurotransmitter secretion. The hypoxic secretory response is totally calcium-dependent, entering cells via high voltage activated (HVA) calcium channels, as it is fully sensitive to dihydropyridines. Whereas the presence of several HVA calcium currents in rat CB has been well documented, the presence of low voltage activated (LVH; T-type channels) has not been reported to date. The fact that O₂-sensitive PC12 cells expresses T-type channels and that they are inducible by hypoxia leaded us to hypothesize they could play a role in CB chemoreceptor cells hypoxic response.

In the present work we analyze the expression of the three isoforms of T-type calcium channels (alpha1G, 1H and 1I) in rat CB by RT-PCR and immunocitochemistry. We demonstrate the presence of the a1G subunit co-localizing with tyrosine hydroxylase (a chemoreceptor cell marker) and define their expression changes (qPCR) after exposure to CH in vivo. Finally, we demonstrate the participation of LVH in rat CB hypoxic activation because their pharmacological inhibition blocks by 50% hypoxia-induced secretory response without affecting high potassium-induced secretion. These results lead us to conclude that rat CB express T-type Ca ²⁺ channels that are active on hypoxia-evoked response. Support: BFU2004-06394, CIBER CB06/06/0050, FISS PI042462, JCyL VA011C05.