Acetylcholine Elevates Intracellular Ca ²⁺ Via Muscarinic and Nicotinic Receptors in Rat Carotid Body Type I Cells

Abstract

Acetylcholine (ACh) has been proposed to act as an excitatory neurotransmitter on sensory nerve endings (reviewed in Fidone & González, 1986) in the carotid body. However, several facts undermine this hypothesis, particularly the species-dependence of its effects and the apparent absence of cholinergic receptors on afferent terminals of the carotid sinus nerve. In contrast, both nicotinic and muscarinic receptors abound in type I and type II cells (Dinger et al, 1985, 1986). Consequently, although the evidence for a post-synaptic role for ACh is questionable, there is good evidence for a pre-synaptic role, which would account for the high ACh-sensitivity of the discharge frequency of the sinus nerve (Monti-Bloch & Eyzaguirre, 1980). We have therefore investigated the effects of ACh on Ca²⁺ signalling in freshly isolated single type I cells.