Slow cardioacceleration mediated by noncholinergic transmission in the stellate ganglion of the cat.
In C1-spinal, pentobarbital-anaesthetized or anemically decerebrated cats, the preganglionic input to the acutely decentralized right stellate ganglion was stimulated with 10- to 30-s strains at 20-40 Hz. Electrical stimulation consistently produced an increase in heart rate in the presence of blocking doses of hexamethonium and atropine or after depletion of acetylcholine from the preganglionic axons by prolonged low frequency stimulation in the presence of hemicholinium. The increase in heart rate had a delayed slow onset, lasted several minutes, and was abolished by propranolol or by section of the inferior cardiac nerve. The magnitude and duration of the heart rate increase were related to intensity, frequency, and duration of preganglionic stimulation. The response to stimulation of a given white ramus was progressively attenuated, and eventually irreversibly lost, during prolonged continuous stimulation of that ramus, while the response to stimulation of a different unstimulated ramus was unchanged. We conclude that the slow cardioacceleration results from a slow and prolonged excitation of postganglionic neurons by a noncholinergic transmitter released by the preganglionic axons.
D000818:Animals; D002415:Cats; D003655:Decerebrate State; D004558:Electric Stimulation; D005260:Female; D006339:Heart Rate; D018738:Hexamethonium; D006584:Hexamethonium Compounds / Q000494:pharmacology; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D013233:Stellate Ganglion / Q000502:physiology*; D009435:Synaptic Transmission; D013997:Time Factors
D006584:Hexamethonium Compounds; D009270:Naloxone; D018738:Hexamethonium