Atropine does not abolish cephalic vagal stimulation of gastrin release in dogs

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Abstract
The effect of atropine was studied on serum gastrin responses to feeding in conscious gastric fistula dogs. Intragastric pH was monitored and could be maintained at pH 6.0 by infusion of sodium bicarbonate into the gastric fistula. A standard liquid meal was consumed by the dogs in < 1 min. Serum gastrin increased from a basal concentration of 8 to 27 pmol/l at 4-7 min, and intragastric pH fell to < 3.0 after 20 min. Since vagotomy abolished the early gastrin response to feeding and instillation of the meal directly into the fistula produced only a modest and delayed increase in serum gastrin, cephalic vagal stimulation may be important in mediating the gastrin responses. When intragastric pH was maintained at 6.0, serum gastrin was significantly higher at all times from 4-50 min after feeding, indicating the importance of acid inhibition in the control of gastrin secretion. After atropine (25 or 100 .mu.g/kg), acid secretion was abolished and intragastric pH was .apprx. 6.0 at all times. The low dose of atropine enhanced the gastrin response to feeding, but the time course and magnitude of the response closely resembled that to normal meals pH-stated to 6.0. The high dose of atropine decreased, but did not abolish serum gastrin responses to feeding. When the meal was allowed to drain freely from the gastric fistula (virtually eliminating stimulation of gastrin release by luminal mechanisms) serum gastrin again reached a peak after 4-7 min and neither dose of atropine significantly changed the response. Apparently cephalic vagal stimulation of gastrin release is atropine resistant and thus unlikely to be mediated by muscarinic receptors. The enhanced gastrin response to feeding caused by moderate doses of atropine can be attributed to the loss of acid inhibition of gastrin release. The neuropeptide bombesin is a candidate neurotransmitter for the action of post-ganglionic vagal nerves on gastrin cells.