COMPARISON BETWEEN ACTIVATION OF ORNITHINE DECARBOXYLASE AND HISTIDINE-DECARBOXYLASE IN RAT STOMACH

We compared the responses of rat stomach ornithine decarboxylase (ODC) and histidine decarboxylase (HDC) to food intake, oral treatment with antisecretagogues, NaHCO3, and hypertonic NaCl, antrectomy, intraveno us infusion of gastrin-17, the selective cholecystokinin (CCK)-B/gastr in receptor antagonist L-365,260, and the somatostatin analogue RC-160 . The serum gastrin concentration and oxyntic mucosal ODC and HDC acti vities were higher in freely fed rats than in fasted rats. Food intake in fasted rats raised the serum gastrin concentration and the ODC and HDC activities. Ranitidine, omeprazole, and NaHCO3 raised the serum g astrin concentration and activated ODC and HDC. Hypertonic NaCl raised the ODC activity 200-fold, whereas circulating gastrin and HDC activi ty were increased only moderately. Infusion of gastrin-17 activated HD C but not ODC. L-365,260 prevented the activation of HDC but not of OD C in response to food intake and treatment with omeprazole, NaHCO3, or hypertonic NaCl. Antrectomy prevented the food- and omeprazole-evoked rise in oxyntic mucosal HDC activity but not the rise in ODC activity . RC-160 suppressed HDC activity after food intake and treatment with omeprazole, NaHCO3, or NaCl. In contrast, RC-160 suppressed omeprazole - and NaHCO3-evoked ODC activation but not that evoked by food intake or NaCl. The results support the view that HDC in the oxyntic mucosa i s activated by gastrin and suppressed by somatostatin. The induction o f ODC is not mediated;by gastrin; ODC activation appears to be related to acid inhibition per se or to mucosal maintenance and repair; somat ostatin, or rather the lack of it, might contribute to the induction o f ODC after acid blockade. The mechanism behind the activation of rat stomach ODC seems to differ depending on the type of stimulus.