[H-3]tyramine uptake by rat liver slices

Rat liver slices were employed as experimental model to characterise the sy stem involved in the transport process which participates in liver tyramine uptake. The uptake of 0.4 mu mol l(-1) of [H-3]tyramine by rat liver slice s was linear from 5 min up to the end of incubation. At 15 min the uptake w as 4.58 +/- 0.18 pmol mg(-1) protein. The accumulation of [H-3]tyramine was sensitive to temperature (69.3 +/- 4.0% inhibition at 0 degrees C, P < 0.0 01), to sodium omission replaced by 150 mmol l(-1) Tris or 110 mmol l(-1) T ris + 40 mmol l(-1) choline (27.6 +/- 6.0%, P < 0.01, and 24.6 +/- 3.8% inh ibition, P < 0.01, respectively), and the inhibition of Na+-K+-adenosine tr iphosphatase by 150 mu mol l(-1) ouabain (20.4 +/- 2.6% decrease, P < 0.01) . Uptake of [H-3]tyramine was cocaine- (10 mu mol l(-1)) and desipramine- ( 1 mu mol l(-1)) dependent (32.2 +/- 6.4%, P < 0.05, and 31.6 +/- 4.0% inhib ition, P < 0.05, respectively). Uptake of [H-3]tyramine in rat liver slices was not modified by 30 mu mol l(-1) isoprenaline, 30 mu mol l(-1) corticos terone, 30 mu mol l(-1) normetanephrine and noradrenaline up to 4 mu M; at higher noradrenaline concentrations tyramine transport was diminished (P < 0.05). Results achieved by incubation with increasing tyramine concentratio ns indicate that at the micromolar level hepatic uptake occurs by a combine d passive diffusion and transport-mediated mechanism, whereas at greater ty ramine concentrations passive transport predominates. These results suggest that both simple diffusion and a transport-mediated mechanism are involved in this uptake from hepatocytes, which presents features similar to those described for type 1 non-neuronal uptake systems. (C) 1999 Academic Press.