AJP - Gastrointestinal and Liver Physiology, Vol 249, Issue 2 197-G202, Copyright © 1985 by American Physiological Society
Effect of GRP on beta-adrenergic-stimulated gastrin and somatostatin release in the isolated rat stomach
G. M. Short, G. M. Reel, J. W. Doyle and M. M. Wolfe
The present studies were directed toward examining the effects of
gastrin-releasing peptide (GRP) on acid secretion and on
beta-adrenergic-stimulated gastrin and somatostatin release using the
isolated vascularly perfused rat stomach. Including pentagastrin in
perfusion buffer increased acid output from 2.2 +/- 0.4 mueq H+/h during
control perfusion to 18.8 +/- 1.8 mueq H+/h (P less than 0.01). No
significant changes in acid secretion were detected when either GRP or
specific antibodies to GRP were included in perfusate in the absence or
presence of pentagastrin. Inclusion of 10(-9) M isoproterenol in the
perfusate did not change acid output with respect to control; however,
gastrin and somatostatin release into the portal venous effluent was
significantly enhanced. Peak gastrin and somatostatin concentrations
observed at 15 min were 753 +/- 43% (P less than 0.001) and 345 +/- 43% (P
less than 0.01), respectively, of basal levels. When antibodies to GRP were
included in perfusate containing isoproterenol, gastrin and somatostatin
release into the portal venous effluent was significantly inhibited. The
results of these studies indicate that GRP does not affect basal or
pentagastrin-stimulated gastric acid secretion in the isolated perfused rat
stomach. However, under the conditions of these experiments,
beta-adrenergic stimulation of gastrin and somatostatin release appears to
be mediated, at least in part, through GRP.
