• 1 January 1979
    • journal article
    • research article
    • Vol. 288  (MAR) , 411-423
Abstract
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 anesthetized rabbit. High doses of ACh (.gtoreq. 50 .mu.g 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. The muscarinic agonist bethanechol inhibited chemoreceptor activity, an effect which was blocked by high doses of atropine, as was the inhibition casued by ACh. Dopamine-induced inhibition was unaffected by atropine. Atropine, in doses sufficient to abolish the vasodepressor effect of ACh, only slightly reduced the inhibitory action of ACh on the chemoreceptors. The vasodilators sodium nitrite and sodium nitroprusside did not appreciably alter chemosensory discharge. The inhibitory response to ACh may not be secondary to vascular changes. The inhibitory response to dopamine, but not that to ACh, was blocked by the dopamine antagonist .alpha.-flupenthixol. Inhibition of chemosensory activity evoked by exogenous ACh may not be secondary to dopamine release. The implications of the results were discussed, particularly with regard to the possible physiological role of ACh as a modulator of carotid chemosensory activity.