Studies on the putative anticholinergic effects of desmethylimipramine

Desmethylimipramine (DMI) and atropine were compared in a variety of organ system tests in rats and mice involving muscarinic receptor function in order to assess the anticholinergic-like activity of this tricyclic antidepressant drug. DMI was similar to atropine in maximally inhibiting basal gastric acid secretion and markedly protecting against restraint-induced stomach ulceration. It did not, however, substantially increase pupil size, reduce fecal pellet output, inhibit cholinergically induced salivation or specifically antagonize the CNS effects of carbachol and oxotremorine as did atropine. From these data and previous work indicating that DMI acts at a site in the central nervous system to inhibit gastric acid secretion, it is concluded that the biological effects of this drug are not mediated through an atropine-like mechanism.