Augmentation of release of gastric somatostatin-like immunoreactivity by adenosine, adenosine triphosphate and their analogs.

The effect of adenosine, adenosine 5'-triphosphate (ATP) and ATP analogs on basal gastric somatostatin-like immunoreactivity (SLI) release was studied using the vascularly perfused rat stomach. The release of gastric SLI was stimulated by adenosine (0.6-60 microM) concentration dependently, while the release of immunoreactive gastrin was inhibited by 1 and 10 microM adenosine. The stimulatory action of adenosine was probably mediated by adenosine receptors because the receptor antagonist, 8-phenyltheophylline, abolished the action of adenosine. In addition, the adenosine-induced release of SLI was not mediated by a cholinergic or beta-adrenergic mechanism, since atropine, hexamethonium or propranolol did not block the action of adenosine. Dipyridamole enhanced the adenosine-stimulated, but not 2-chloroadenosine-induced SLI release. Since the adenosine analog, 2-chloroadenosine, is resistant to the adenosine uptake mechanism, it is likely that adenosine-stimulated release of gastric SLI is due to the activation of extracellular receptors. ATP also stimulated gastric SLI release. The analogs alpha,beta-methyleneadenosine triphosphate and diphosphate, which are resistant to metabolic breakdown, did not stimulate basal SLI release, while gamma,beta-methyleneadenosine triphosphate, which can be metabolized, increased the release of SLI. In addition, the ATP-induced release of SLI was abolished by 8-phenyltheophylline. Therefore, the action of ATP is likely to be a result of its metabolism to adenosine.