A possible role for catecholamines in carotid body chemoreception

Exogenously administered dopamine (DA) has frequently been reported to depress carotid chemoreceptor activity transiently. Recent evidence supports the presence of DA in high concentrations in the Type I cells of the carotid body (c.b.), and the possibility of its release into the synaptic cleft between the Type I cell and the afferent nerve. We are testing the hypothesis that DA depresses c.b. activity in the cat by activating an adenylate cyclase (a.c.) cAMP system. In 3 experiments a.c. activity in response to sodium fluoride in both the c.b. and the carotid nerve (c.n.) (0.11 and 0.09 nmoles cAMP/mg protein/20 min incubation respectively) was fourfold that under basal conditions. In 3 experiments a.c. activity was found to be 3.5 times greater in the microsomal fraction of the c.b. homogenates than in the mitochondrial fraction. In 5 out of 6 experiments c.b.s transiently perfused in situ with DA during hyperoxia showed more cAMP than the opposite side c.b.s which were removed during hypoxic exposure (8.05 vs. 5.65 pmoles/c.b.). From these results we conclude that an a.c. cAMP system is present in the c.b. and c.n., that brief injections of DA acting in situ appear able to stimulate the system, and that exogenous DA may depress the neural activity of c.b. chemoreception by increasing cAMP in the c.n. This could promote the phosphorylation of a membrane protein and subsequent hyperpolarization (Greengard and Kebabian, Fed. Proc. 33:1059-1067).