Evidence of a cholinergic, pH dependent, vagally mediated release of antral somatostatin

Aliño, S.F.; Garcia, D.; Uvnäs-Moberg, K.

Acta Physiologica Scandinavica. Supplementum 515: 21-27


ISSN/ISBN: 0302-2994
PMID: 6137933
Accession: 005411066

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In anesthetized rats, the stomachs were perfused with dextran solution (pH .apprx. 6) at a rate of 0.035 ml/min. Electrical vagal stimulation (5 V, 5 Hz and 2 ms) increased acid secretion and also the intraluminal secretion of gastrin and somatostatin, as evidenced by a decrease of the perfusate pH from 2.21 to 1.20 and by an increase of gastrin and somatostatin levels from 14 to 108 pg/ml and from 9 to 174 pg/ml, respectively. Pretreatment with hexamethonium, 1 mg/kg, and atropine 0.5 mg/kg, virtually abolished the secretory responses of both gastric acid and the hormonal peptides. During gastric perfusion with 0.05 M HCl (giving rise to an intragastric pH .apprx. 1.45), atropine, 0.5 mg/kg, still inhibited the vagally induced release of gastrin and somatostatin, suggesting that the elimination of the release of gastrin and somatostatin was not a consequence of the absence of gastric acid secretion. Pretreatment of the rats with atropine, 0.05 mg/kg, changed the response pattern to electrical vagal stimulation considerably. Gastric acid secretion was only partly inhibited (pH of the perfusate decreased from 2.98 to 1.75). Somatostatin levels failed to increase, but gastrin levels increased from 0 to 755 pg/ml, i.e., about an 8-fold increase in comparison with control experiments. When the lowest dose of atropine (0.02 mg/kg) was given. pH of the perfusate dropped from 3.14 to 1.44 and the release of somatostatin appeared to return, as evidenced by an increase of the perfusate somatostatin levels, from 2 to 83 pg ml. The output of gastrin (0-677 pg/ml) was about 7-fold increased when compared to control experiments. The inhibition of the vagally released somatostatin caused by low doses of atropine implies that this vagal effect is mediated by cholinergic fibers. The finding of a greatly exaggerated gastrin response, when the release of somatostatin was blocked by atropine, suggests that the vagally controlled intraluminal gastrin secretion is mediated by noncholinergic fibers and that, under normal circumstances, the release of gastrin is under inhibitory control. I.v. infusions of carbachol, 60 .mu.g/kg per h, and urecholine, 600-1200 .mu.g/kg per h, stimulated acid secretion as evidenced by a fall in perfusate pH from 2.91 to 1.41 and from 3.21 to 1.44. Gastrin levels increased from 3 to 432 and 0 to 254 pg/ml and somatostatin levels from 7.5 to 158 and 0 to 196 pg/ml.