The Carotid Body (CB) stands as a prototypical organ specialized in acute oxygen (O2) sensing, orchestrating reflexive hyperventilation and heightened cardiac output during instances of hypoxemia. The recurrence of intermittent hypoxia generates a repetitive stimulus that potentially triggers CB overactivation, contributing to the sympathetic hyperactivity observed in sleep apnea sufferers. Despite evidence showcasing the malleability of CB function due to chronic intermittent hypoxia (CIH), the intricate mechanisms underpinning this phenomenon remain partially understood. This study unveils that CIH elicits a modest expansion in CB dimensions and prompts a reconfiguration of cell types within the CB structure. Notably, this involves the mobilization of latent, immature neuroblasts, which embark upon a journey of differentiation, ultimately transforming into mature, O2-sensing, neuron-like chemoreceptor glomus cells. Through the prospective isolation of distinct cell classes, we demonstrate that as CB neuroblasts mature, there is a concurrent surge in the expression of specific genes associated with acute O2-sensing in glomus cells. Furthermore, CIH enhances the hypoxia-responsive capacity of mitochondria both in the progressing neuroblasts and the established glomus cells. This novel insight into the mechanisms governing CB-mediated sympathetic overflow offers a fresh perspective and the potential for the development of innovative pharmacological interventions with implications for sleep apnea patients.
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