Salivation induced by prostaglandin F2α and modification of the response by atropine and physostigmine

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Abstract
1 Administration of PGF2α to the anaesthetized dog produced dose-related salivation accompanied by weak pressor and negative cardiac chronotropic effects. Injection of PGE1 did not produce salivation. 2 Electrical stimulation of the chorda tympani nerve or injection of PGF2α produced salivary responses which were not affected by pretreatment with phentolamine, but were abolished by pretreatment with atropine. Treatment with hexamethonium reduced the response to nerve stimulation but did not alter the response to PGF2α. 3 Pretreatment with physostigmine augmented the salivary response to both nerve stimulation and PGF2α. 4 These experiments suggest that salivation produced by PGF2α is probably due in part, to liberation of acetylcholine from cholinergic nerve terminals. These results are consistent with previously proposed modulatory functions of prostaglandins on neurotransmission.

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