Chronic hypoxia (CH) and chronic intermittent hypoxia (CIH) induce carotid body (CB) chemoreceptors sensitization. It has been suggested that reactive oxygen species (ROS) contribute to the genesis of this sensitization. CIH mimics sleep apneas, with the recurrent apneas-rebreathing mimicking ischemia-reperfusion episodes. Our aim was to determine the extent of CB sensitization in CH and CIH and define the significance of ROS in this process. We have used four groups of animals for each hypoxic situation: normoxic (control), hypoxic, and normoxic and hypoxic supplemented with an antioxidant diet. Hypoxia means 15 days in a 10-11% O₂ atmosphere (CH) and 80s normoxia + 40s hypoxia (10-11% O₂), 30 times/h, 8h/day (CIH). We monitored ventilation and CB catecholamine (CA) metabolism and several ROS-related parameters. CBs from CH rats have higher CA content, synthesis rate and turnover time; antioxidant supplementation in CH leads to a drop in a content, an increase in synthesis rate and a decrease in turnover time.

CBs from CH rats had an increased release response to acute hypoxic and high K⁺ tests, both in control and antioxidant-supplemented rats. CH increased ROS production and antioxidant supplementation reversed the pro-oxidant status to nearly normoxic levels. It is concluded that CH generates an status of oxidation that modifies CB CA-storing and synthesizing capacity but does not affect the sensitivity to hypoxia, indicating that ROS are not involved in the sensitization process observed in CH. Data from CIH would also be provided. Support: BFU 2004-06394, CIBER CB06/06/0050, FISS PI042462, JCyL VA045/04 and VA011C05