Alpha-bungarotoxin binding in cat carotid body.

The carotid body is an arterial chemosensory organ which detects changes in blood gas tensions and pH, and reflexly contributes to the cardiorespiratory adjustments which occur during hypoxia, hypercapnia and acidosis. However, the sensory mechanisms involved in carotid chemoreception remain to be elucidated. Morphologically, the carotid body consists of an association of elemental units, or glomeruli, within a connective tissue stroma penetrated by a dense capillary net 5. The glomeruli are comprised of catecholamine-rich type I, or chief cells, which are enveloped by glial-like processes of type II, or sustentacular, cellsa,4,19. Sensory fibers from the carotid sinus nerve penetrate the glomeruli to terminate in synaptic-like apposition on type I cellst,18, 21. Schweitzer and Wright 25 first noted the stimulatory effects of acetylcholine (ACh) on carotid chemoreflexes in the cat, and suggested that this substance might be involved in the generation of chemosensory activity. Later experiments characterized in detail the excitatory potency of ACh and nicotinic agonists on the chemoreceptor discharge from the cat carotid body 7,9,10,24. They showed that cholinergic antagonists abolish the sensitivity to ACh and reduce the response to natural stimulation. More recently , it has been demonstrated that chemically identifiable ACh is present in the pa-renchymal tissue of the cat carotid body, rather than in the fibers or terminals of the carotid sinus nerve11,l~, 15. Although the site(s) of ACh storage in this tissue has not been firmly established, a high affinity component of choline uptake has been autora-diographically localized to the type I cells 12. Finally, there is evidence that ACh is released from the carotid body during natural stimulationS,L One interpretation of these findings is that ACh is a sensory transmitter in the cat carotid body, and that as such, this substance is released from the type I cells by natural stimulation to activate nico-tinic receptors on neighboring sensory nerve terminals, thereby leading to the initiation of chemosensory impulses in the carotid sinus nerve 1°. Other recent studies have shown, however, that ACh directly depolarizes the type I cells in both normal and de-* To whom correspondence should be addressed.