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.
Functional control of gastrin releasing peptide (GRP) mRNA in rat stomach
