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Hypoxia-induced secretion of serotonin from intact pulmonary neuroepithelial bodies in neonatal rabbit

X. W. Fu , C. A. Nurse*, V. Wong and E. Cutz

We examined the effects of hypoxia on the release of serotonin (5-HT) from intact neuroepithelial body cells (NEB), presumed airway chemoreceptors, in rabbit lung slices, using amperometry with carbon fibre microelectrodes. Under normoxia (P_O2 ~155 mmHg; 1 mmHg 133 Pa), most NEB cells did not exhibit detectable secretory activity; however, hypoxia elicited a dose-dependent (P_O2 range 95-18 mmHg), tetrodotoxin (TTX)-sensitive stimulation of spike-like exocytotic events, indicative of vesicular amine release. High extracellular K⁺ (50 mM) induced a secretory response similar to that elicited by severe hypoxia. Exocytosis was stimulated in normoxic NEB cells after exposure to tetraethylammonium (20 mM) or 4-aminopyridine (2 mM). Hypoxia-induced secretion was abolished by the non-specific Ca²⁺ channel blocker Cd²⁺ (100 µM). Secretion was also largely inhibited by the L-type Ca²⁺ channel blocker nifedipine (2 µM), but not by the N-type Ca²⁺ channel blocker -conotoxin GVIA (1 µM). The 5-HT₃ receptor blocker ICS 205 930 also inhibited secretion from NEB cells under hypoxia. These results suggest that hypoxia stimulates 5-HT secretion from intact NEBs via inhibition of K⁺ channels, augmentation of Na⁺-dependent action potentials and calcium entry through L-type Ca²⁺ channels, as well as by positive feedback activation of 5-HT₃ autoreceptors.

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