Antral somatostatin interacts with gastric acid secretion. We aimed to investigate the effect of eradication on gastric acid, somatostatin secretion and mucosal histology in gastric ulcer patients with Helicobacter pylori (H. pylori) infection.

Twenty-eight patients (21 male, 7 female) with H. pylori-positive gastric ulcer were treated with dual therapy. Before and 4-8 weeks after the therapy, the histology of biopsy specimens, basal acid output (BAO) and maximal acid output (MAO) after stimulation with tetragastrin were assessed. Somatostatin concentration in the gastric juice was measured by radioimmunoassay, and somatostatin output during either the basal or gastrin-stimulated period was also examined.

Eradication was successful in 22 patients. Before treatment, the acid and somatostatin output were inversely related to the severity of neutrophil infiltration in the corpus and antrum, respectively. After successful eradication, improvement of histological inflammation and an increase in BAO, basal and gastrin-stimulated somatostatin output were observed. Eradication had no effect on atrophy and MAO. There was a positive correlation between gastric acid and somatostatin output in the basal or stimulated condition, irrespective of H. pylori infection.

The present results suggest that recovery of gastric BAO may be caused by an improvement in corpus neutrophil infiltration, but not by an increase in parietal cell volume or a change in atrophy. Also, there was an increase in basal and gastrin-stimulated somatostatin-containing cell activity accompanied by improved antral neutrophil infiltration in the early phase after H. pylori eradication in gastric ulcers.

Pirenzepine has inhibitory effects on gastrin secretion both in vivo and in vitro. The aim of this study was to determine the mechanism responsible for the suppression of omeprazole-induced hypergastrinemia that occurs with pirenzepine treatment. The effects were measured in rats treated with oral omeprazole plus intraperitoneal pirenzepine or saline once daily for seven days in the antrum. The serum gastrin level increased significantly by more than sixfold with omeprazole treatment; additional treatment with pirenzepine suppressed this increase by 48%. Pirenzepine treatment did not change the level of gastrin mRNA but significantly increased the level of somatostatin mRNA. Combination treatment with omeprazole plus pirenzepine significantly decreased the gastrin mRNA level to half and significantly increased the somatostatin mRNA level up to 1.4-fold of the levels achieved with omeprazole treatment alone. These results suggest that the stimulatory effect of omeprazole on gastrin synthesis is partially blocked by pirenzepine via mediation of somatostatin synthesis in the antrum.

Using antibodies to a complementary peptide of somatostatin, putative somatostatin binding proteins were characterized on canine parietal cells. A synthetic peptide (S-C1) was derived from the complementary mRNA sequence for somatostatin-14. Antiserum containing antibodies to S-C1 inhibited competitively 125I-Tyr11-somatostatin binding to canine oxyntic mucosal membranes. Canine parietal cell preparations were incubated with carbachol in the presence or absence of somatostatin and antisera to S-C1. Antibodies to S-C1 produced a decrease in carbachol-stimulated 14C-aminopyrine uptake comparable with that produced by 10(-6) M somatostatin. In immunocytochemical studies by light microscopy, antibodies to S-C1 produced positive staining of parietal cells throughout the oxyntic gland area. By electron microscopy using immunogold techniques, binding by antibodies to somatostatin C-1 was localized ultrastructurally to basolateral and intracellular membranes and to secretory canalicular membranes of parietal cells. These studies support the conclusion that antibodies to the somatostatin complementary peptide demonstrate properties similar to those of somatostatin in that they inhibit carbachol-stimulated aminopyrine uptake and 125I-somatostatin binding. Furthermore, these antibodies localize to specific regions on plasma membranes of parietal cells, which may represent somatostatin binding sites.