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

Abstract

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 the neurotransmitters release. ATP released by CBs glomus cells 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 hours) cellular and molecular mechanisms (first 24 hours) in CBs, as well as the effects of short-term SH on populations of glomus cell are still poorly understood. Herein, we show that SH (10% O₂ for 24 hours) 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 the two glomus cell subpopulations differently. 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 hours of SH, which may contribute to the generation of cardiovascular and ventilatory adjustments observed in this experimental model.