The presynaptic component of a cholinergic mechanism in the carotid body chemotransduction of hypoxia in the cat.

Abstract

In the past we have shown that cholinergic blockers given together or singly could greatly reduce the carotid body’s response to a perfusion of hypoxic Krebs Ringer bicarbonate solution (KRB) (Fitzgerald & Shirahata, 1994; Fitzgerald et al, 1995). The operating model in those studies was transmission in the superior cervical ganglion. That is, the Type I cell of the carotid body was analogous to the presynaptic neuron; it contained acetylcholine (ACh). In fact the Type I cell has been identified as the source of ACh in several different studies. The synthesizing enzyme, choline acetyltransferase (ChAT), has been located there (Ballard & Jones, 1972; Wang et al, 1989). Fidone et al (1977) have located the high affinity sodium-dependent choline uptake transporter in the Type I cells. They have also reported that carotid bodies which had been denervated contained as much ACh as their intact counterparts (Fidone et al, 1976), suggesting that the extensive innervation in the carotid body and the very few ganglia reported to be there contribute an immeasurably small amount of ACh. And we (Goldberg et al, 1978) analyzed the carotid sinus nerve directly to find no appreciable amount of ACh in it.