The mediation of increased duodenal alkaline secretion in response to 10 mM HCl in the anaesthetized rat. Support for the involvement of capsaicin-sensitive nerve elements.

Experiments were performed on chloralose-anaesthetized rats. Bicarbonate secretion by the duodenal mucosa was continuously recorded by use of an in situ-titration technique. Exposing the duodenal segment to 10 mM HCl over 5 min increased the bicarbonate transport by about 65%. This acid-induced secretory response was resistant to neural decentralization by means of bilateral cervical vagotomy and/or splanchnicotomy. Furthermore, in the decentralized state, serosal application of the local anaesthetic lidocaine or tetrodotoxin (TTX) lowered basal duodenal bicarbonate secretion. Despite the presence of lidocaine or TTX, exposure of the duodenal mucosa to 10 mM HCl induced a net increase in secretion with a magnitude similar to that observed in the control situation with intact nerves. A 5-min exposure period of the decentralized duodenal segment to capsaicin (1.2 mg ml-1) raised bicarbonate secretion, a response which also occurred in the presence of lidocaine (serosa). Tachyphylaxis to capsaicin blocked the secretory response to 10 mM HCl and inhibited the response to luminal prostaglandin E2 (1.5 10(-5) M) by 80%. The present results indicate that luminal exposure to 10 mM HCl activates capsaicin-sensitive primary afferents which, locally within the submucosa or epithelium, activate the bicarbonate secretion.