Adrenaline Stimulates Acid Production in Isolated Pig and Human Parietal Cells

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Abstract
To investigate the mechanisms of adrenergic stimulation of the parietal cell and to study the possible relationship between the stress hormone adrenaline and duodenal ulcer, the effects of adrenaline and various adrenoceptor agonists and antagonists were investigated in parietal cells isolated from pig stomachs and from endoscopic biopsy specimens taken from the gastric mucosa of patients. Parietal cell acid production was assayed by the aminopyrine accumulation technique. Adrenaline as the sole drug showed poor or no stimulatory effect but potentiated histamine-stimulated acid production. In the presence of histamine, beta-adrenoceptor agonists caused a stimulation of acid formation with the potency order isoproterenol>adrenaline>noradrenaline. The beta-2-selective antagonist ICI118551 was a more potent inhibitor of acid production than both the beta-1 antagonist practolol and the H2-receptor antagonist cimetidine. Studies of (3H)-dihydroalprenolol (DHA) binding to purified parietal cell membranes showed a protein-concentration-dependent and specific binding of 2.2 .+-. 0.6 pmol DHA/.mu.g. Adrenaline increased gastric acid production in both pig and human parietal cells, most likely through a beta-2 receptor on the parietal cell. The adrenaline stimulatory effect in cells obtained from patients wtih peptic ulcer was more pronounced than in cells from non-ulcer patients, which indicates a possible role of adrenaline in some types of ulcer disease.