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First published online on January 18, 2002.
 Copyright © 2002 by The Physiological Society
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Received August 7, 2001
Accepted after revision November 30, 2001

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

X.W. Fu1, C.A. Nurse2, V. Wong1, and E. Cutz3*

1 Division of Pathology, Department of Pediatric Laboratory Medicine, The Hospital for Sick Children, The Research Institute and University of Toronto, Toronto, Ontario, Canada M5G 1X8
2 Department of Biology, McMaster University, Hamilton, Ontario, Canada L8S 4K1
3 Division of Pathology, Department of Pediatric Laboratory Medicine, The Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8

* To whom correspondence should be addressed. E-mail: ernest.cutz{at}sickkids.ca.

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 (PO2 ~155 mmHg; 1 mmHg 133 Pa), most NEB cells did not exhibit detectable secretory activity; however, hypoxia elicited a dose-dependent (PO2 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 {omega}-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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