Beta-adrenergic regulation of cyclic adenosine 3‘,5’ monophosphate accumulation in human gastric epithelial glands. Inhibitory effect of somatostatin

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Abstract
The action of catecholamines and somatostatin on cyclic adenosine 3′,5′ monophosphate (cyclic AMP) formation in human isolated gastric glands is reported. We show that: (1) there is a beta 2 receptor-mediated stimulation of cyclic AMP production in fundus. Catecholamines act with the order of potencies isoproterenol (ED50= 50 nmol l-1) > epinephrine (ED50= 0·1 μmol l-1) > norepinephrine (ED50= 5 μmol l-1). Their action is completely reversed by propranolol at doses 103 times lower than practolol, while unaffected by phentolamine; (2) isoproterenol and Vasoactive Intestinal Peptide (VIP) have additive effects on cyclic AMP in fundic glands whereas no additivity is observed between histamine and isoproterenol; this, together with the absence of catecholamine effect in antral glands, suggests that the beta 2 receptor is located on parietal cells; (3) somatostatin (1 μmol l-1) non-competitively inhibits the stimulation by catecholamines but does not affect VIP and histamine stimulations. These results suggest a physiological stimulatory effect of catecholamines on gastric acid secretion in man, through a beta 2 receptor coupled to the cyclic AMP system, regulated by somatostatin.