Afferent chemoreceptor activity was recorded from the peripheral
cut end of the sinus nerve in anaesthetized cats and rabbits. It was
found that intracarotid injection of dopamine inhibited spontaneous
chemoreceptor activity in both species. 5~Hydroxytryptamine evoked
a brief excitation followed by inhibition of discharge in both species.
In cats, apomorphine caused a prolonged inhibition of chemoreceptor
activity. Following administration of a~flupenthixol or haloperidol
in cats and a-f1upenthixol in rabbits, dopamine no longer evoked an
inhibitory response but instead tended to cause an increase in chemo¬
receptor discharge. Responses to the chemoreceptor stimulants sodium
cyanide and hypoxia were potentiated following administration of
dopamine-blocking agents. These results suggest the possibility
that endogenous dopamine acts to depress afferent carotid chemoreceptor
activity.
Subsequent experiments in cats showed that the dopamine-uptake
blockers benztropine and nomifensine, but not the monoamineoxidase
inhibitor pargyline, potentiate the inhibitory action of injected
dopamine and also potentiate chemoreceptor responses to sodium
cyanide and hypoxia. These results imply that, in addition to its
inhibitory action, endogenous dopamine has an excitatory action on
chemoreceptor activity. It is suggested that the most likely
physiological role for dopamine in the carotid body is as a chemical
mediator in an 'amplification' system, modulating activity in sensory
nerve endings which are themselves the chemoreceptors.
Injection of acetylcholine in rabbits caused inhibition of
afferent chemoreceptor activity, in contrast to the stimulation
evoked in cats and dogs. In some experiments high doses of acetylcholine evoked a slight excitation which preceded the inhibition.
This effect was probably brought about by an action on nicotinic
receptors since it was blocked by mecamylamine but is unlikely to be
of physiological significance. The muscarinic agonists methacholine
and bethanechol, but not the nicotinic agonist subery1dicholine,
also inhibited spontaneous chemoreceptor discharge indicating that
the inhibition was brought about by an action on muscarinic receptors.
The inhibition was blocked by atropine, although high doses were
required to produce this effect. The inhibition is unlikely to be
a consequence of a vascular action of acetylcholine since the vaso¬
dilator drugs sodium nitrite and sodium nitroprusside had little
effect on chemoreceptor activity. The inhibition evoked by acetyl¬
choline was not reduced by a-f1upenthixol and is, therefore, unlikely
to be secondary to dopamine release. It is proposed that acetylcholine
may act as a transmitter in an inhibitory efferent pathway to the
carotid body but is unlikely to act as an excitatory sensory transmitter
