New theory for receptor mechanism of carotid body chemoreceptors

Abstract

EVER since De Castro¹ first ascribed a chemosensory function to the carotid body (later confirmed by Heymans, et al.²), there has been much discussion and controversy over the precise mechanism whereby stimulation of the afferent fibres is achieved^3,4. The controversy initially centred around the nature of the neurotransmitter released by the glomus cell, which was assumed to be highly sensitive to hypoxia and less sensitive to hypercapnia and acidaemia. Perhaps the most generally accepted theory was that the glomus cells respond to hypoxia by releasing a neurotransmitter that initiates an increase in firing rate of the nerve fibres terminating on the glomus cells. The afferent nature of these fibres was originally deduced by De Castro⁵ from light microscopic examination of the nerve fibres innervating the carotid body. The early ultrastructural studies, however, failed to show clear evidence of afferent types of nerve ending in synaptic contact with the glomus cells. On the contrary, these nerve endings were purported to be presynaptic and therefore efferent in function because they contain large numbers of agranular ‘synaptic’ vesicles^6–8. This conclusion was further substantiated by Biscoe et al.⁹, who showed that intracranial decentralisation of the IXth cranial nerve caused degeneration of nerve endings on glomus cells. These findings led to an alternative theory of chemoreceptor action³. In this case the chemosensory function is attributed to numerous free nerve endings of small diameter, which are found in the carotid body tissue. The glomus cells and associated nerves are held to form part of an efferent inhibitory feedback system, in which release of biogenic amines, that are known to be present in large quantities in glomus cells, depresses chemoreceptor activity.