PARTICIPATION OF NA-BODY CHEMORECEPTOR CELLS TO HYPOXIA( CHANNELS IN THE RESPONSE OF CAROTID)

The role played by Na+ channels of carotid body (CB) chemoreceptor cel ls was investigated by studying the effects of tetrodotoxin (TTX) on t he release of H-3-labeled catecholamines ([H-3]CA) by adult rabbit CBs previously incubated with the precursor [H-3]tyrosine. TTX inhibited partially the release of [H-3]CA elicited by mild hypoxia (10 or 7% O- 2) or by depolarizing incubation medium containing 20 or 30 mM KCl, bu t the response to more intense hypoxia (5 or 2% O-2) or to higher KCl concentration (40 or 50 mM) was not significantly affected. The releas e of [H-3]CA elicited by acidic stimuli, either 20% CO2 (pH 6.6) or th e protonophore dinitrophenol (100 mu M), although comparable in magnit ude to that elicited by mild hypoxia, was not modified by TTX. These r esults provide evidence for the first time that Na+ channels of chemor eceptor 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 O-2-sensitive K+ c hannels. Sympathetic denervation of CBs was followed by a marked reduc tion in the release of [H-3]CA elicited by veratridine or by 20 mM KCl , suggesting that the number of Na+ channels in chemoreceptor cells de creases after denervation.