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• W2329419785 abstract "Pulmonary neuroepithelial bodies (NEB) in mammalian lungs are thought to function as airway O 2 sensors that release serotonin (5-HT) in response to hypoxia. Direct evidence that NEB cells also respond to airway hypercapnia/acidosis (CO 2 /H + ) is presently lacking. We tested the effects of CO 2 /H + alone or in combination with hypoxia on 5-HT release from intact NEB cells in a neonatal hamster lung slice model. For the detection of 5-HT release we used carbon fiber amperometry. Fluorescence Ca 2+ imaging method was used to assess CO 2 /H + -evoked changes in intracellular Ca 2+ . Exposure to 10 and 20% CO 2 or pH 6.8–7.2 evoked significant release of 5-HT with a distinct rise in intracellular Ca 2+ in hamster NEBs. This secretory response was dependent on the voltage-gated entry of extracellular Ca 2+ . Moreover, the combined effects of hypercapnia and hypoxia were additive. Critically, an inhibitor of carbonic anhydrase (CA), acetazolamide, suppressed CO 2 /H + -mediated 5-HT release. The expression of mRNAs for various CA isotypes, including CAII, was identified in NEB cells from human lung, and protein expression was confirmed by immunohistochemistry using a specific anti-CAII antibody on sections of human and hamster lung. Taken together our findings provide strong evidence for CO 2 /H + sensing by NEB cells and support their role as polymodal airway sensors with as yet to be defined functions under normal and disease conditions." @default.
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• W2329419785 date "2015-04-15" @default.
• W2329419785 modified "2023-10-18" @default.
• W2329419785 title "Pulmonary neuroepithelial bodies are polymodal airway sensors: Evidence for CO₂/H⁺sensing" @default.
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• W2329419785 doi "https://doi.org/10.1152/ajplung.00208.2014" @default.
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