Inhibition by somatostatin of carbamylcholine-induced gastrin and glucagon release from the isolated perfused canine stomach.

At an arterial plasma concentration of 61 nmol/l (100 ng/ml) synthetic cyclic somatostatin completely abolished basal glucagon and gastrin release as well as carbamylcholine-induced glucagon and gastrin release from the isolated perfused dog stomach. These observations are compatible with the view that endogenous somatostatin previously reported to be released during vagal stimulation might be involved to explain the lack of gastric-glucagon response in this situation. They do not, however, rule out the alternative proposal that the dog fundic A-cell may simply be a non-innervated cell.