AbstractCarotid 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 (R0) of glomus cells. Sliced carotid bodies (for cell visualization) of cats, rabbits, and mice were used.The mean Emand R0of rabbit glomus cells were lower than those of cat and mouse. R0of mouse cells was the largest, whereas Ermswas 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+]0and Mn2+), reduced their resistance, and induced variable changes in Erms. Different ACh doses produced non‐linear effects on ΔEm. Nic and BN also depolarized most cells, reducing R0and Erms. Atropine depressed the cell responses to BN; α‐bungarotoxin the depolarizing response to Nic. ME and SP depolarized most cells, but only ME significantly reduced R0. 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 R0. There were negative correlations between ΔEmand ΔR0with the cholinergics and SP; correlations between ΔErmsand ΔR0were 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 t