A decrease in arterial PO₂ causes an inhibition of K⁺ channels in carotid body chemoreceptor cells (CBCC). Cell depolarization, Ca²⁺ entry, release of neurotransmitters and increased activity in the CB sensory nerve follow. Reactive Oxygen Species (ROS) may act as oxygen-sensing mediators in CBCC. Mitochondrial respiratory chain is a major source of ROS with the glutathione redox pair being their main cellular buffer. We have measured the glutathione redox potential of the cells (EGSH) in relationship with the CBCC activity, assessed as the release of catecholamines (CA), in three experimental situations: 1) using mitochondrial venoms; 2) different PO₂; 3) and presence of reducing and oxidizing agents. The mitochondrial venoms, electron transport chain inhibitors (Rotenone, 3-Nitropropionic Acid, Antimicyn A, Sodium Azide) and the uncoupler Dinitrophenol induce the activation of the CBCC independently of the effect on EGSH that they produce.

Using several PO₂, from hypoxia to hyperoxia we found that only intense hypoxia (8mm Hg) and hyperoxia (630 mm Hg) significantly decreased the EGSH. Because hypoxia increases and hyperoxia inhibits the CA release, there is not a relationship between the redox status and the activity of CBCC induced by modifying PO₂. The reducing (NAC, NMPG, GSH) and oxidizing agents (PCMBS, DTNA, DIA, GSSG, BSO, BCNU, AT) tested, showed the same lack of correlation. These discrepancies suggest that CBCC response to the variation of PO₂ is not affected by the general redox potential (EGSH) of the cells. Support: BFU2004-06394, CIBER CB06/06/0050, FISS PI042462, JCyL VA045/04 and VA011C05