Abstract
Chronic intermittent hypoxia (CIH) induces carotid body plasticity manifested as sensory long term facilitation (sLTF). CIH‐induced sLTF requires reactive oxygen species (ROS) signaling. Mice partially deficient in the transcriptional activator hypoxia‐inducible factor‐2α subunit (Hif‐2α+/‐) exhibit oxidative stress and augmented carotid body sensitivity to hypoxia, which are similar to CIH‐exposed wild‐type mice. We hypothesized that Hif‐2α deficiency would evoke sLTF of the carotid body due to increased ROS levels. Consistent with this possibility, Hif‐2α+/‐ mice displayed sLTF compared to their wild type littermates and systemic administration of the membrane permeable antioxidant MnTMPyP prevented both oxidative stress as well as sLTF. CIH decreased Hif‐2α protein levels in the carotid body and induced oxidative stress. Blocking CIH‐induced HIF‐2α degradation by ALLM treatment inhibited ROS generation and prevented CIH‐evoked sLTF in rats. Taken together, these results suggest that Hif‐2α degradation in response to CIH is a critical molecular mechanism leading to ROS‐dependent induction of carotid body sLTF. Supported by NIH‐ HL‐90554.
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