title: Effects of Putative Neurotransmitters of the Carotid Body on its Own Glomus Cells.
abstract: Carotid body glomus cells produce and release acetylcholine (ACh), catecholamines, and neuropeptides, and there is biochemical evidence that these cells possess receptors for these substances. Thus, we studied the effects of cholinergics [ACh, nicotine (Nic), bethanechol (BN)] and peptides [met-enkephalin (ME), substance P (SP)] on the membrane potential (Em), voltage noise (Erms), and input resistance (Ro) of glomus cells. Sliced carotid bodies (for cell visualization) of cats, rabbits, and mice were used. The mean Em and Ro of rabbit glomus cells were lower than those of cat and mouse. Ro of mouse cells was the largest, whereas Erms was similar in all species. The various agents had qualitatively similar effects on the cells of the three species although some quantitative differences were sometimes observed. But, for simplicity, results were pooled. ACh depolarized most cells (effect depressed by zero [Ca2+]o and Mn2+), reduced their resistance, and induced variable changes in Erms. Different ACh doses produced non-linear effects on DeltaEm. Nic and BN also depolarized most cells, reducing Ro and Erms. Atropine depressed the cell responses to BN; alpha-bungarotoxin the depolarizing response to Nic. ME and SP depolarized most cells, but only ME significantly reduced Ro. Neither peptide significantly changed voltage noise. Comparing the effects of all drugs showed that BN was the most effective depolarizing agent, producing the largest reductions in Ro. There were negative correlations between DeltaEm and DeltaRo with the cholinergics and SP; correlations between DeltaErms and DeltaRo were significant and positive only with the cholinergics. These results confirm the presence of nicotinic, muscarinic, and peptidergic receptors in glomus cells. The similar effects of cholinergics and peptides and those of flow interruption and anoxia suggest that the latter may partly act via autoreceptors for the released transmitters.
authors.affiliation: Department of Physiology, University of Utah School of Medicine, Salt Lake City, UT 84108, USA.
authors.forename: C.
authors.initials: C
authors.lastname: Eyzaguirre
authors.forename: L.
authors.initials: L
authors.lastname: Monti-Bloch
authors.forename: J. W.
authors.initials: JW
authors.lastname: Woodbury