Cods were equipped with cannulae for drainage of the stomach and for the separate perfusion of the stomach (pure seawater containing phenol red as a volume marker) and intestine (diluted seawater). Acidity of the gastric effluence was titrated, its volume calculated from the phenol red concentration. Gastric mucosal plasma flow (MPF) was estimated by gastric 14C-aniline clearance. I.m. injection of angiotensin II (AII) depressed basal acid secretion in a dose-dependent fashion. Also the MPF was reduced, but relatively less than the secretory depression. Therefore, the AII-induced secretory inhibition could not be explained by restrained mucosal blood flow. Perfusion of the intestine with diluted seawater, or a continuous i.m. infusion of 0.6% NaCl both rendered the fishes non-drinking. A high dose of AII (150 micrograms/kg . h) induced drinking in intestinally perfused cod while lower doses (15, 50 micrograms/kg . h) did not. In i.m. saline-injected cod, all three doses were dipsogenic. The results suggest that 0.6% saline infusion induces a permanent satiety and that intestinal perfusion in addition induces a preabsorptive satiety. The preabsorptive satiety appears more resistant to the dipsogenic action of AII than the permanent one.