In vivo studies in the pig showed no net loss or gain of endogenous porcine gastrin during transport across the liver in fasting animals. Infusion of synthetic human heptadecapeptide gastrin (G-17) in doses of 0,25, 0,5 and 1,0 microgram/kg/min raised circulating gastrin levels to those found in the postprandial state. At no time was there a loss or gain of immunologically determined gastrin across the liver. Changes in the molecular size of gastrin, however, suggested that qualitative but not quantitative effects followed the administration of G-17 in vivo. The disappearance of gastrin from the circulation was biphasic, with an initial half-life of 3 minutes and a slower phase suggesting recirculation or multicompartment equilibration. The distribution at equilibrium was +/- 20% of body weight calculated from arterial levels, but 30-40% if portal or hepatic venous values were used. The mean blood production rate was +/- 125 microgram/day but the portal contribution was only 30 microgram/day, suggesting an important alternative source of gastrin.