Pulmonary neuroepithelial bodies are polymodal airway sensors:

doi:10.1152/ajplung.00208.2014.—Pulmonary neuroepithelial bodies (NEB) in mammalian lungs are thought to function as airway O2 sensors that release serotonin (5-HT) in response to hypoxia. Direct evidence that NEB cells also respond to airway hypercapnia/acidosis (CO2/H) is presently lacking. We tested the effects of CO2/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 Ca2 imag-ing method was used to assess CO2/H-evoked changes in intracel-lular Ca2. Exposure to 10 and 20 % CO2 or pH 6.8–7.2 evoked significant release of 5-HT with a distinct rise in intracellular Ca2 in hamster NEBs. This secretory response was dependent on the voltage-gated entry of extracellular Ca2. Moreover, the combined effects of hypercapnia and hypoxia were additive. Critically, an inhibitor of carbonic anhydrase (CA), acetazolamide, suppressed CO2/H