Intracellular signalling in arterial chemoreceptors during acute hypoxia and glucose deprivation: role of ATP

• DOI: 10.1113/jp287130
• Publication Date: 2025-02-12T18:29:11Z
• Authors: María Torres‐López; Patricia González...; Olalla Colinas; Hee‐Sool Rho; Hortensia Torres‐...; Antonio Castellano; Lin Gao; Patricia Ortega‐S...; José López‐Barneo
• Keywords: Glomus cell; Hypoxia

Abstract The carotid body (CB) is the main oxygen (O 2 ) sensing organ that mediates reflex hyperventilation and increased cardiac output in response to hypoxaemia. Acute O an intrinsic property of CB glomus cells, which contain special mitochondria generate signalling molecules (NADH H modulate membrane K + channels lowered tension (hypoxia). In parallel with these membrane‐associated events, cells are highly sensitive mitochondrial electron transport chain (ETC) inhibitors. It was suggested a decrease oxidative production ATP critical event mediating hypoxia‐induced cell depolarization. Here, we show rotenone [an inhibitor complex (MC) I] activates rat mouse but abolishes their responsiveness hypoxia. Rotenone does not prevent further activation by cyanide (a blocker MCIV) or glucose deprivation. Responsiveness deprivation enhanced ‐insenstive genetic disruption MCI. These findings suggest acute requires functional MCI intracellular ATP, presumably produced simultaneous inhibition MCIV, involved hypoxia signalling. support this concept, levels single were unaltered hypoxia, rapidly declined following exposure low inhibitors phosphorylation. observations indicate reduction participate physiological sensing. However, local decreases glycolytic origin may contribute cells. image Key points contains oxygen‐sensitive specialized inhibit Glomus blockers. signal inducing channel depolarization ETC blockade. Rotenone, I, (an MCIV blocker) Single‐cell decreased 0 mM A it hypoglycaemia