Alpha‐2 agonists by an effect on alpha‐2 adrenoreceptors in the stomach (and probably in the brain also) suppress vagal nerve acetylcholine release thereby inhibiting gastric motility and secretion and inhibiting the development of gastric lesions in rats in the stress‐, reserpine‐, and cysteamine‐induced ulcer models. Since the effects of the alpha‐2 agonists are consistently inhibited by alpha‐2 blocking agents, their effects appear to be selectively mediated via the alpha‐2 receptor. It seems appropriate therefore that the role of the alpha‐2 receptors be recognized in studies of gastric function and ulcer development.
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Taylor et al. (1982) studied this question.
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