1. Intracarotid (I.C.) injection of either acetylcholine (ACh) or dopamine inhibited spontaneous chemosensory activity recorded from the peripheral cut end of the sinus nerve in the anaesthetized rabbit. 2. High doses of ACh (greater than or equal to 50 micrograms I.C.) evoked a slight increase in discharge which preceded the inhibition. This excitation was attributable to a nicotinic action of the drug since it was abolished by mecamylamine. 3. The muscarinic agonist bethanechol inhibited chemoreceptor activity, an effect which was blocked by high doses of atropine, as was the inhibition caused by ACh. Dopamine-induced inhibition was unaffected by atropine. 4. Atropine, in doses sufficient to abolish the vasodepressor effect of ACh, only slightly reduced the inhibitory action of ACh on the chemoreceptors. Also, the vasodilators sodium nitrite and sodium nitroprusside did not appreciably alter chemosensory discharge. It seems unlikely, therefore, that the inhibitory response to ACh is secondary to vascular changes. 5. The inhibitory response to dopamine, but not that to ACh, was blocked by the dopamine antagonist alpha-flupenthixol. This implies that inhibition of chemosensory activity evoked by exogenous ACh was not secondary to dopamine release. 6. The implications of the results are discussed, particularly with regard to the possible physiological role of ACh as a modulator of carotid chemosensory activity.