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Beta‐adrenergic regulation of cyclic adenosine 3‘,5’ monophosphate accumulation in human gastric epithelial glands. Inhibitory effect of somatostatin
Author(s) -
BOIGE N.,
DUPONT C.,
CHENUT B.,
GESPACH C.,
ROSSELIN G.
Publication year - 1984
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1984.tb00702.x
Subject(s) - medicine , endocrinology , adenosine , somatostatin , practolol , chemistry , phentolamine , stimulation , histamine , propranolol , biology
. 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 (ED 50 = 50 nmol l ‐1 ) > epinephrine (ED 50 = 0·1 μmol l ‐1 ) > norepinephrine (ED 50 = 5 μmol l ‐1 ). Their action is completely reversed by propranolol at doses 10 3 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.