Ammonium chloride (30 mumol/min/kg bw), lactate (50 mumol/min/kg bw) or ammonium chloride plus lactate were infused for two hours into the mesenteric vein of sheep. Blood samples were taken before, during, and two hours after infusion from portal, hepatic and jugular veins for estimation of ammonia, urea, lactate and glucose. Average portal and hepatic blood flow was 59 +/- 35 and 89 +/- 48 ml/min/kg bw respectively without any regular changes when ammonium chloride or lactate alone were administered. The treatment with ammonium chloride increased the hepatic ammonia fixation from 9.1 +/- 2.1 to 25.2 +/- 5.7 mumol/min/kg bw and urea formation from 17.6 +/- 14.2 to 56.4 +/- 43.2 mumol/min/kg bw. The infusion of ammonium chloride alone provoked a peripheral hyperammonaemia and it increased the endogenous sources of ammonia for urea production. Both lactate and ammonia caused an increase of hepatic glucose release. It was suggested that lactate stimulated mainly gluconeogenesis, and ammonium-glucogenolysis. The effect of ammonia in the last reaction as well as an increased net urea formation in the liver, was probably mediated by the hypoinsulinaemia and/or an increase of adrenaline secretion.