Abstract
Pulmonary neuroepithelial bodies (NEBs), occurring as densely innervated groups of neuroendocrine cells in the airway epithelium, are believed to be receptor–effector units ideally positioned to respond to changes in air composition. Acute hypoxia is suggested to close background K+ channels in NEB cells, resulting in plasma membrane depolarisation, voltage-gated Ca2+ entry and transmitter release. However, no conclusive evidence is available because physiological studies are hampered by the relatively small number and dispersed distribution of NEBs in the lung, making them almost unreachable for direct measurements and manipulation, and by the lack of reliable in vitro models.
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