AJP - Cell Physiology, Vol 267, Issue 3 C738-C744, Copyright © 1994 by American Physiological Society
Participation of Na+ channels in the response of carotid body chemoreceptor cells to hypoxia
A. Rocher, A. Obeso, M. T. Cachero, B. Herreros and C. Gonzalez
Departamento de Bioquimica y Biologia Molecular y Fisiologia, Facultad de Medicina, Universidad de Valladolid, Spain.
The role played by Na+ channels of carotid body (CB) chemoreceptor cells
was investigated by studying the effects of tetrodotoxin (TTX) on the
release of 3H-labeled catecholamines ([3H]CA) by adult rabbit CBs
previously incubated with the precursor [3H]tyrosine. TTX inhibited
partially the release of [3H]CA elicited by mild hypoxia (10 or 7% O2) or
by depolarizing incubation medium containing 20 or 30 mM KCl, but the
response to more intense hypoxia (5 or 2% O2) or to higher KCl
concentration (40 or 50 mM) was not significantly affected. The release of
[3H]CA elicited by acidic stimuli, either 20% CO2 (pH 6.6) or the
protonophore dinitrophenol (100 microM), although comparable in magnitude
to that elicited by mild hypoxia, was not modified by TTX. These results
provide evidence for the first time that Na+ channels of chemoreceptor
cells participate in the transduction of hypoxic stimuli into the
neurotransmitter release response of these cells and suggest that Na+
current operates as an amplifying device that enhances the initial cell
depolarization mediated by the closure of the O2-sensitive K+ channels.
Sympathetic denervation of CBs was followed by a marked reduction in the
release of [3H]CA elicited by veratridine or by 20 mM KCl, suggesting that
the number of Na+ channels in chemoreceptor cells decreases after
denervation.
