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Atropine does not abolish cephalic vagal stimulation of gastrin release in dogs
Author(s) -
Dockray G. J.,
Tracy Hilda J.
Publication year - 1980
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1980.sp013408
Subject(s) - atropine , gastrin , endocrinology , medicine , stimulation , chemistry , gastric acid , sham feeding , vagotomy , g cell , stomach , secretion
1. 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. 2. A standard liquid meal was consumed by the dogs in less than a minute. Serum gastrin increased from a basal concentration of 8 pmol/l to a peak of 27 pmol/1 at 4‐7 min, and intragastric pH fell to less than 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, we conclude that cephalic vagal stimulation played a major part in mediating the gastrin responses. When intragastric pH was maintained at 6·0 serum gastrin was significantly higher at all times from 4 to 50 min after feeding, indicating the importance of acid inhibition in the control of gastrin secretion. 3. After atropine (25 or 100 μg/kg), acid secretion was abolished and intragastric pH was about 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. 4. 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. 5. It is concluded that cephalic vagal stimulation of gastrin release is atropine resistant and so 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.