Purinergic control of gastric somatostatin release

Depending on the animal species, adenosine has been show to inhibit gastric acid secretion directly by acting on parietal cells or indirectly by releasing somatostatin, an acid inhibitor. The objective of the present study is to examine if adenosine augments the release of somatostatin in the isolated vascularly perfused mouse stomach. Results show that the selective A 2A receptor agonist (CGS 21680) stimulated while the selective A 1 receptor agonist (CPA) inhibited gastric somatostatin release. The stimulatory effect of CGS 21680 was concentration dependent. In addition, the adenosine‐stimulated somatostatin release was abolished by the administration of the selective A 2A receptor antagonist (ZM 241385), but not by the A 1 receptor antagonist (DPCPX). In conclusion, the present experiments show that the release of gastric somatostatin in the mouse is under purinergic controls. Adenosine exerts both stimulatory and inhibitory actions on somatostatin. It is conceivable that adenosine may exert its acid inhibitory effect on the mouse stomach by stimulating predominantly the release of somatostatin via the activation of adenosine A 2A receptors. (Supported by Wah Sheung Fund).