A comparative physiological and pharmacological study of cat and rabbit carotid body chemoreceptors.

Carotid bodies and their nerves were excised from rabbits or cats, cleaned of surrounding connective tissue and placed in a chamber through which mammalian saline equilibrated with different gas mixtures was allowed to flow. Single fibers were isolated and identified as chemosensory by their response to hypoxia, hypercapnia, or NaCN. Mass receptor potentials (recorded at some distance from the sensory nerve endings) were evoked by the same stimuli and registered as close as possible to the carotid body. Both cats and rabbits exhibited receptor depolarization and an increased discharge in response to NaCN, hypoxia, hypercapnia and cyanide. However, the effects of some pharmacological agents were quite different in rabbits and cats. In the rabbit, ACh 10-100 microgram and carbachol 1-10 microgram produced receptor hyperpolarization and discharge depression followed by discharge increase. Nicotine 0.3-20 microgram induced receptor depolarization and increased chemosensory discharge frequency. Nicotinic stimulation was antagonized by D-tubocurarine 10(-6)-10(-4) g/ml. Pilocarpine 2-50 microgram hyperpolarized the receptors and depressed discharge frequency. Pilocarpine-induced depression was reduced by atropine 10(-6) g/ml. Dopamine 5-100 microgram depolarized the receptors and increased the chemosensory discharge frequency. This effect of dopamine was reduced by haloperidol (10(-11)-10(-7) M). In the cat, ACh, carbachol and nicotine (same doses as those used in rabbits) induced receptor depolarization and increased the sensory discharge frequency. Pilocarpine (up to 50 microgram) had little effect on either discharge frequency or the receptor potential. Dopamine 5-100 microgram induced receptor hyperpolarization and depression of discharge frequency, and these effects were reduced by haloperidol.