Pharmacological evidence for the existence of a neuronal amine uptake mechanism in the dog liver in vivo

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Abstract
The possibility of a neuronal uptake mechanism in the liver was studied in dogs anesthetized with sodium pentobarbital. Plasma catecholamine concentrations in hepatic venous blood were determined by a radioenzymatic assay following injections of tyramine (30–1000 μg) into either the common hepatic artery or the portal vein. Concomitant changes in hepatic vascular parameters and aortic catecholamine concentrations were also investigated. The mean basal values for hepatic venous and aortic catecholamine concentrations were found to be 0.081 ± 0.007 ng/mL and 0.433 ± 0.080 ng/mL, respectively. Injections of tyramine (300 and 1000 μg) into the hepatic artery increased hepatic venous catecholamine concentrations significantly to 0.109 ± 0.017 ng/mL and 0.126 ± 0.023 ng/mL (P < 0.05. n = 7), respectively. Hepatic arterial vascular conductance decreased concomitantly by 29.7 and 44.9% (P < 0.05, n = 7), respectively. Intraportal injections of tyramine did not bring about significant changes in either hepatic venous catecholamine concentrations or portal venous vascular conductance at any dose tested. After inhibition of monoamine oxidase with pargyline (10 mg/kg. i.v.), the effects of tyramine (1000 μg) injected into the hepatic artery were potentiated. The duration of action was approximately 10 min after pargyline pretreatment (control duration: 1 min). The effects of tyramine were absent after inhibition of the neuronal uptake mechanism with desipramine (1 mg/kg. i.v.). No drug tested had a significant effect on aortic catecholamine concentrations. The present results support the presence of the neuronal uptake mechanism in the dog liver.