Short-term sustained hypoxia distinctly affects subpopulations of carotid body glomus cells from rats.

The main O2 arterial chemoreceptors are the carotid bodies (CBs), which mediate hyperventilation in response to short-term sustained hypoxia (SH). CBs contain glomus cells expressing K+ channels, which are inhibited by hypoxia, leading to neurotransmitter release. ATP released by CBs and type II cells has been considered essential for chemosensory processing under physiological and pathophysiological conditions. Although the systemic effects of chronic activation of CBs by SH are well known, the early (first 24 h) cellular and molecular mechanisms in CBs as well as the effects of short-term SH on populations of glomus cells are still poorly understood. Here, we show that SH (10% O2 for 24 h) depolarizes the membrane potential of one population of glomus cells, mediated by increases in inward current, but does not affect the ATP release by CBs. In addition, SH promotes a reduction in their maximum outward current, mediated by voltage-gated K+ channels. SH also affected sensitivity to acute hypoxia in one glomus cell subpopulation. As for the content of mitochondrial proteins, we observed increases in the citrate synthase, Tom-20, and succinate dehydrogenase (mitochondrial complex II) per cell of CBs after SH. Our results demonstrate important cellular and molecular mechanisms of plasticity in CBs from rats after only 24 h of SH, which may contribute to the generation of cardiovascular and ventilatory adjustments observed in this experimental model.NEW & NOTEWORTHY Our study revealed two subpopulations of glomus cells of carotid bodies (CBs) with specific electrophysiological properties, which were differentially affected by short-term sustained hypoxia (SH; 10% O2 for 24 h). Our experiments showed that SH also affected the sensitivity to acute hypoxia of these glomus cell subpopulations differently. Our molecular analyses allowed us to identify important adaptations in the content of CB mitochondrial proteins that participate in the Krebs cycle and form the electron transport chain.