The pharmacology, pharmacokinetics, clinical efficacy, adverse reactions, drug interactions, and dosage of
ranitidine are reviewed; specific comparisons are made of this new H2-receptor antagonist with the older agent,
cimetidine.
Ranitidine is a potent inhibitor of gastric acid secretion whose chemical structure lacks the
imidazole group previously believed to be essential for H2-receptor blocking activity. The new agent does not bind substantially to the
cytochrome P-450 mixed-function oxidase system and does not penetrate the cerebrospinal fluid appreciably. Peak serum
ranitidine concentrations occur within one to two hours after
oral administration; approximately 50% of an oral dose reaches systemic circulation. There are at least three metabolites of
ranitidine, but substantial fractions of both i.v. and oral doses are recovered unchanged in the urine.
Ranitidine's duration of action is 8-12 hours. Controlled clinical trials have shown
ranitidine to be effective in the treatment of duodenal and
gastric ulcers,
Zollinger-Ellison syndrome, and prophylaxis against aspiration during
anesthesia.
Ranitidine has been effective in patients unresponsive to or intolerant of
cimetidine. In clinical trials, the incidence of adverse effects from
ranitidine has been low; certain rare but serious side effects that have been noted with
cimetidine have not been associated with
ranitidine therapy. There is no evidence thus far that certain
drug-drug interactions observed with
cimetidine therapy will occur with
ranitidine. Oral adult daily doses of
ranitidine are likely to be 300 mg given as the hydrochloride
salt in two divided doses.
Ranitidine is similar to
cimetidine in efficacy but has an apparently safer adverse-effects profile.
Ranitidine is likely to be the preferred agent in certain clinical situations.