Abstract
The mechanism by which prostaglandin F 2α (PGF 2α) produces salivation has been further characterized. Intraarterial injection of PGF 2α (0.05–0.5 μg) or acetylcholine (10–100 μg) produced dose-related salivation. Treatment with atropine (30 μg, i.a.) shifted the dose-response curve for acetylcholine to the right in parallel fashion, but shifted the response curve for PGF 2α to the right in non-parallel fashion. Tetrodotoxin (12 μg, i.a.) antagonized salivation induced by chorda tympani nerve stimulation and by PGF 2α, while the response to exogenous acetylcholine remained unaltered. PGF 2β produced salivation but was considerably less potent than PGF 2α. 15-epi PGF 2α did not produce salivation. Chronic decentralization of the chorda shifted the dose-response curve for PGF 2α to the left. Saliva produced by stimulation of the chorda or by infusion of PGF 2α (4 μg/kg/min) was slightly alkaline, rich in sodium, and contained low concentrations of potassium and total protein. These results are consistent with the previous suggestion that PGF 2α produces salivation by liberation of endogenous acetylcholine.
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