The methods available for assaying ranitidine in plasma and both the drug and its metabolites in urine are high-performance liquid chromatography and radioimmunoassay. Following oral administration, the absorption of ranitidine in normal individuals has been found to be rapid, with peak plasma concentrations occurring at 1 to 3 hours. Peak plasma concentrations bear a constant relationship to dose, but vary widely between individuals. The bioavailability of ranitidine after oral administration is approximately 50% due to presystemic hepatic metabolism. Plasma protein binding of ranitidine is approximately 15% and the apparent volume of distribution is greater than body volume. Ranitidine penetrates very poorly into the cerebrospinal fluid but is concentrated into breast milk. After intravenous administration, plasma concentrations decay in a biexponential manner. The elimination half-life is almost 2 hours and is somewhat longer after oral administration. Plasma clearance is approximately 600 ml/min of which most is renal clearance. Elimination of ranitidine is not dose-dependent. Hepatic metabolism is the other major route of elimination and there may be some enterohepatic recycling of the drug. Food has no effect on the kinetics of ranitidine but concurrent administration of antacids reduces its absorption. Renal disease causes an increase in ranitidine plasma concentrations through reduced clearance and possibly increased bioavailability. Chronic liver and some reduction in clearance. In the elderly, there is a reduction in clearance and prolongation of the elimination half-life but little effect on bioavailability. There is a relationship between plasma concentrations of ranitidine and suppression of gastric acid production but wide interindividual variability.