Regulation of gastric somatostatin secretion in the mouse by luminal acidity: a local feedback mechanism

Gastroenterology. 1988 Feb;94(2):317-22. doi: 10.1016/0016-5085(88)90418-0.


The present study was designed to determine whether somatostatin secretion induced by histamine or pentagastrin in the isolated luminally perfused mouse stomach was a direct effect of the secretagogues on gastric somatostatin cells or an indirect effect mediated by the increase in luminal acidity. Perfusion of the lumen with exogenous acid (80-480 nmol/min) caused an increase in somatostatin secretion in proportion to the increase in luminal acidity. The increase in somatostatin secretion was resistant to tetrodotoxin and attained maximal levels (61.6% +/- 8.7% above basal level) similar to those elicited by maximal doses of secretagogues. Conversely, neutralization of basal acid secretion with bicarbonate (20-160 nmol/min) caused a decrease in somatostatin secretion in proportion to the decrease in luminal acidity. Similarly, neutralization of the secretagogue-induced increments in acid secretion with bicarbonate or inhibition of the increments with cimetidine abolished the corresponding increments in somatostatin secretion. It is proposed that acid-induced release of somatostatin in proximity to parietal cells serves as a negative feedback mechanism restraining acid secretion.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Bicarbonates / pharmacology
  • Cimetidine / pharmacology
  • Feedback
  • Gastric Acid / metabolism
  • Gastric Acid / physiology*
  • Gastric Mucosa / metabolism*
  • Histamine / pharmacology
  • Hydrogen-Ion Concentration
  • Male
  • Mice
  • Pentagastrin / pharmacology
  • Somatostatin / metabolism*


  • Bicarbonates
  • Somatostatin
  • Cimetidine
  • Histamine
  • Pentagastrin