Inhibitory effect of somatostatin on gastric acid secretion in rats.

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Abstract
Effects of somatostatin on parasympathetically induced increases in gastric acid secretion and mucosal blood flow (MBF) were studied in anethesized rats with a gastric fistula. Intravenous blood infusion of small doses of somatostatin (0.1-0.5 .mu.g/kg/min) dose-dependently inhibited the increases in the vagally stimulated gastric acid secretion. Larger doses of somatostatin (0.5-2.5 .mu.g/kg/min) also dose-dependently inhibited the benthanechol-induced gastric acid secretion. The dose of somatostatin required to inhibit the gastric acid secretion by about 50% of the preinfused control values were 0.25 .mu.g/kg/min for vagally stimulated acid secretion and 2.5 .mu.g/kg/min for bethanechol-induced acid secretion. Thus, the inhibitory potency of somatostatin on the vagally stimulated acid secretion was about 10-fold higher than that on bethanechol-induced acid secretion. Somatostation had no effect on the increase in gastric MBF during vagal nerve stimulation or bethanechol infusion. Pretreatment with indomethacin or phentolamine had no effect on the inhibitory effect of somatostatin on the increase in gastric acid secretion during vagus nerve stimulation or bethanechol infusion. These results suggest that somatostatin exerts an inhibitory effect on gastric acid secretion by acting on the parasympathetic neurons in the gastric wall more than on the structures peripheral to the parasympathetic nerve terminals, and it reduces parasympathetically stimulated gastric acid secretion in rats. This inhibitory effect of somatostation on the gastric acid secretion is independent of the changes in the gastric MBF and probably not related to prostaglandin-involved or alpha adreneceptor-mediated mechanisms.