Distention-induced gastrin release: effects of luminal acidification and intravenous atropine.
We evaluated whether gastric distention with saline test meals could release gastrin in healthy subjects and whether luminal acidification or atropine would modify this response. Distention with 700 ml saline adjusted to pH 5.0 led to a significant gastrin response (averaging 9 +/- 3 pg/ml above basal levels during the first 15 min after distention, P less than 0.02), whereas distention with 25 ml saline led to no gastrin release. Distention with 700 ml saline adjusted to pH 2.5 also led to a significant gastrin rise, which was nearly identical to that seen at pH 5.0. A small dose of atropine (2.3 micrograms/kg i.v.) significantly enhanced the gastrin response to 700-ml distention at pH 5.0 (average gastrin rise 20 +/- 3 pg/ml, P less than 0.02 vs. 700 ml without atropine). This enhancement of gastrin release by atropine was not due to changes in intragastric pH, because pH was held constant at 5.0 by in vivo intragastric titration. Enhancement was also not due to greater gastric distention after atropine, because gastric volumes after the 700-ml test meal were similar with or without atropine. Although atropine enhanced distention-induced gastrin release, atropine reduced acid secretion by more than 50% (P less than 0.05). Our findings indicate (a) that gastric distention releases significant amounts of gastrin in healthy subjects; (b) this gastrin response is resistant to inhibition by luminal acidification to pH 2.5 and (c) the gastrin response to distention is enhanced by atropine, suggesting that distention may also activate cholinergic pathways that inhibit gastrin release.
D000328:Adult; D001285:Atropine / Q000494:pharmacology*; D005260:Female; D013271:Gastric Dilatation / Q000378:metabolism*; D005755:Gastrins / Q000378:metabolism*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D012965:Sodium Chloride
D005755:Gastrins; D012965:Sodium Chloride; D001285:Atropine