The effects of nicotine on basal and stimulated gastric secretions in the conscious cat and in isolated guinea pig gastric mucosal cells.

Intravenous (i.v.) administration of nicotine in conscious cats significantly stimulated basal gastric acid output. The effect was completely blocked by atropine and ranitidine. Submaximally stimulated gastric acid secretion was not further increased by nicotine. In isolated guinea pig parietal cells nicotine significantly increased basal acid secretion by about 20% and potentiated the response to maximally effective concentrations of histamine but had no influence on the carbachol response. In isolated parietal cells stimulated either by nicotine, histamine or both, atropine pretreatment increased or inhibited the acid response in concentration-dependent manner. From these data, it is concluded that nicotine had direct stimulatory effects on isolated parietal cells and potentiated the histamine mediated response in the isolated cell preparation but not in the intact animal model.