Involvement of Capsaicin-sensitive Neurons in Gastrin Release Provoked by Intragastric Administration of Bile Salts in the Rat

To clarify the mechanism of gastrin release provoked by the reflux of bile juice into the stomach, we studied the effects of tetrodotoxin (0.08 mg/kg), atropine sulfate (0.5 mg/kg), truncal vagotomy, and chemical denervation of afferent sensory neurons with capsaicin (100 mg/kg) on gastrin release induced by bile salts in the rat (n = 6 per group). Sodium taurocholate and deoxycholate (> 2.5 mM) significantly increased the serum levels of gastrin. However, sodium tauroursodeoxycholate had no effect. The levels of serum gastrin before and 1 h after administration of 2.5 mM sodium taurocholate were 94.6 +/- 10.7 and 211.0 +/- 21.1 pg/ml, respectively. Tetrodotoxin and atropine sulfate completely inhibited this sodium taurocholate induced-gastrin increase, while truncal vagotomy was without effect. Capsaicin markedly reduced the increasing effects of sodium taurocholate. These findings suggested that the neuronal pathways involved in gastrin release are probably an intragastric local circuit originating from capsaicin-sensitive afferent sensory neurons and terminating in muscarinic receptors in the postsynaptic efferent cholinergic neuron system.