ACTIVITY OF THE SPLANCHNIC NERVE AND CAROTID CHEMORECEPTORS IN THE ORIGIN OF PRESSOR RESPONSES TO ACETYLCHOLINE

¹ Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, Texas

In atropine-treated dogs under pentobarbital anesthesia, acetylcholine (ACh) stimulated pre- and postganglionic sympathetic nerve activity coincident with the initial phase of the biphasie pressor response. Compound P-286, in doses sufficient to reverse the pressor response to ACh, markedly reduced this increased nerve activity without affecting spontaneous postganglionic impulses which were readily abolished by chlorisondamine.

Since the postganglionic activity provoked by ACh apparently was of preganglionic origin, consideration was given to the chemoreceptors as possible loci of excitation. The initial phase of the pressor response, produced by injecting ACh into the brachiocephalic artery, was reversed by circulatory isolation of the carotid bodies. When ACh was injected into an aortic arch-brachiocephalic bypass, the initial pressor response was abolished but not reversed by carotid body isolation.

Additional studies demonstrated that the respiratory stimulation from ACh and nicotine was suppressed by P-286 without enhancing the response to cyanide, whereas hexamethonium blocked the stimulation from ACh and nicotine while enhancing that to cyanide. This evidence further differentiates P-286 from typical ganglionic blocking agents and favors the chemoreceptors as sites of ACh action.

It is proposed that the initial pressor phase from intravenous ACh results from chemoreceptor stimulation and the secondary phase from direct stimulation of the adrenal medulla.