Effects of chemoreceptor stimulating agents on reflex bradycardia.

Effects of carotid body chemoreceptor stimulation on reflex bradycardia were studied by injecting various pharmacological and physiological agents into the external carotid artery of rabbits. Reflex bradycardia was induced by ACh and nicotine in doses from 3 micrograms to 10 micrograms. The response to ACh was markedly potentiated by physostigmine and small doses of atropine, while it was completely blocked bymecamylamine and a large dose of atropine. The nicotine-induced bradycardia was also inhibited by mecamylamine and a large dose of atropine. After reserpinization, the responses to ACh and nicotine were depressed, but were elicited by increasing the doses. NaCN, low pH solution and high CO2 saline induced weaker bradycardiac responses which were not affected by atropine and mecamylamine, but were abolished in the reserpinized animals. The results indicate possible participation of dopamine in the chemoreceptor transmission.