Neurogenic control of release of gastrin and somatostatin.

In cats electrical vagal stimulation leads to an atropine-resistant release of gastrin. Hexamethonium on the other hand blocks the release response. These data suggest that at least one noncholinergic and one cholinergic neuron are involved in the vagal pathway innervating the gastrin producing cells. Exogenously administrated somatostatin also inhibits the vagally induced release of gastrin. Vagal stimulation decreases the levels of somatostatin in portal blood, suggesting that a release of gastric somatostatin, occurring during basal conditions, is inhibited. It is therefore possible that the vagally induced release of gastrin is in part secondary to the decreased somatostatin secretion. In contrast, electrical stimulation stimulates the release of gastrin as well as that of somatostatin into the antral lumen. However, the intraluminal release of these peptides only occurs in the presence of low antral pH. In rats, low doses of atropine (0.05 mg/kg) completely inhibits the intragastric vagally mediated release of somatostatin, which leads to an approximately 10-fold enhancement of the simultaneously occurring gastrin release. The intraluminally released somatostatin most likely derives from pH sensitive antral D cells of the open type. The vagal innervation of this population of somatostatin producing cells appears to be cholinergic. Activation of the sympathetic nervous system inhibits the vagally induced release of gastrin dependently of the prevailing antral pH. This inhibitory effect is probably exerted by a neurogenic mechanism at the ganglionic level. In contrast, basal gastrin release is enhanced by activation by the sympathoadrenal system.(ABSTRACT TRUNCATED AT 250 WORDS)