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Human gastric mucosal adenylate cyclase activity: effects of various cytoprotective prostaglandins
Author(s) -
SIMON BERND,
KATHER HORST
Publication year - 1980
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.1365-2362.1980.tb02089.x
Subject(s) - cyclase , prostaglandin , adenylate kinase , cytoprotection , gastric mucosa , prostacyclin , endocrinology , prostaglandin e , medicine , chemistry , prostaglandin e2 , gastric acid , prostaglandin d2 , enzyme , biochemistry , biology , secretion , stomach , apoptosis
. Several prostaglandins prevent ulcer formation (called cytoprotection) by a mechanism other than inhibition of gastric acid secretion. One suggestion is that they increase cyclic AMP in non‐parietal cells. A variety of prostaglandins with potent cytoprotective properties were tested for their capacity to modulate adenylate cyclase activity in homogenates of human gastric mucosa. Prostaglandin E2, prostacyclin (PGI 2 ) and 15(S)‐methyl‐PGE 2 stimulated the cyclase in human gastric mucosal biopsy specimens in a dose‐dependent manner. Cytoprotective prostaglandins without antisecretory properties such as PGF2 β were also able to activate the enzyme system dose‐depen‐dently. In contrast, cytoprotective prostaglandins such as PGD 2 , the PGE 1 ‐analogue, SC‐29333, and the pro‐staglandin‐like compound C 83 did not stimulate human gastric adenylate cyclase. Whereas PGD 2 did not modulate enzyme activity at all, SC‐29333 and C 83 , at concentrations greater than 10 µmol/l, inhibited basal and PGE 2 ‐stimulated enzyme activities. These studies suggest that cyclic AMP is not directly related to the cytoprotective effect of prostaglandins, at least in human gastric mucosa.