Contribution of inflammation on carotid body chemosensory potentiation induced by intermittent hypoxia.

Exposure to chronic intermittent hypoxia (CIH) produces hypertension. A critical process involved in the CIH-induced hypertension is the potentiation of the carotid body (CB) chemosensory responses to acute hypoxia. The CIH-induced changes in the CB chemosensory process have been related to an enhanced reactive oxygen species (ROS) production. However, it is still a matter of debate where ROS could directly modify the CB chemosensory discharge. Recently, we found that CIH-induced increase expression of TNF-a and IL-1b within the CB. Thus, we studied the contribution of these pro-inflammatory cytokines on the enhanced CB chemosensory response to acute hypoxia in rats exposed to CIH. To study the role of TNF-a and IL-1b, male Sprague-Dawley rats were submitted to CIH (5% O(2), 12 times/hr for 8 hr/day) and received chronic ibuprofen treatment (40 mg/kg). Following 21 days of CIH, rats were anaesthetized and the CB chemosensory discharge was recorded in response to several levels FiO2 (5-100%). Exposure to CIH significantly increases the immunorreactive levels of TNF-a and IL-1b in the CB, along with an increase accumulation of the p65 NF-kb subunit. Treating rats with ibuprofen significantly prevents the CIH-induced increases in TNF-a and IL-1b in the CB chemoreceptor cells but failed to decrease the enhanced CB chemosensory reactivity to hypoxia. Our results suggest that the mechanisms underlying the potentiation of the CB chemosensory response to acute hypoxia are not linked to the increased expression of TNF-a and IL-1b within the CBs of CIH-exposed rats.