Cyclic adenosine monophosphate cAMP -stimulated acid secretion

Intracellular cyclic adenosine monophosphate (cAMP)-stimulated add secretion in the isolated guinea-pig gastric mucosa was not inhibited by administration of an H2-receptor antagonist, as expected, although H 83/69 (timoprazole) induced a dose-dependent inhibition. This was the first experimental evidence for a site of inhibitory action beyond the panel of stimulatory cell membrane receptors. Interestingly, it was found that the initial lead compound (CMN 131), had no inhibitory effect on dibutyryl-cAMP-stimulated acid secretion, nor was it an H2-receptor antagonist [9],... 

In close proximity to the parietal cells are gut endocrine cells called enterochromaffin-like (ECL) cells. ECL cells have receptors for gastrin and acetylcholine and are the major source for histamine release. Histamine binds to the H2 receptor on the parietal cell, resulting in activation of adenylyl cyclase, which increases intracellular cyclic adenosine monophosphate (cAMP). cAMP activates protein kinases that stimulate acid secretion by the H+/K+ ATPase. In humans, it is believed that the major effect of gastrin upon acid secretion is mediated indirectly through the release of histamine from ECL cells rather than through direct parietal cell stimulation. 

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