SummaryCimetidine has been shown to stimulate prolactin secretion after intravenous administration. Cimetidine 200 mg and ranitidine 50 mg was given i.v. in a randomly allocated order to 22 volunteers on consecutive days; these doses can be regarded as equivalent as far as inhibition of gastric acid output is concerned. Plasma prolactin was estimated at regular intervals. The prolactin stimulating effect of cimetidine was confirmed while ranitidine did not influence plasma prolactin levels.Although cimetidine and ranitidine seem to be equally effective in reducing gastric acid output, the effect of the drugs are not the same on their entire spectrum of action since ranitidine does not influence plasma prolactin.It still has to be established in clinical trials which drug is the best choice in clinical medicine. IntroductionIntravenous administration of cimetidine stimulates prolactin secretion (Burland et al., 1979;Carlson and Ippoliti, 1977) whereas oral cimetidine treatment in conventional doses does not influence the basal or releasing hormone-stimulated values of prolactin, thyroid-stimulating hormone and luteinizing hormone (Nelis and van de Meene, 1980). A newly synthesized histamine H2-receptor antagonist ranitidine (Glaxo AH 19065) has recently been entered into controlled clinical trials at the Sophia Ziekenhuis.Peden, Saunders and Wormsley (1979) demonstrated a dose-dependent reduction in nocturnal and pentagastrin-stimulated acid output after intra-duodenal instillation of ranitidine. The reduction in acid output after 80 mg ranitidine was comparable to the effect of 400 mg cimetidine. Domschke, Lux and Domschke (1979) showed a comparable effect after i.v. infusion of ranitidine; in this study ranitidine was 4 times more effective than cimetidine on a molar base. A dose of 50 mg ranitidine and 200 mg cimetidine was therefore used in this trial.

Summary IntroductionCimetidine is one of the successes of this decade.