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  • Title: [3H]Tyramine uptake by rat liver slices.
    Author: Tchercansky DM, Rubio MC, Acevedo C.
    Journal: Pharmacol Res; 1999 Jun; 39(6):479-86. PubMed ID: 10373246.
    Abstract:
    Rat liver slices were employed as experimental model to characterise the system involved in the transport process which participates in liver tyramine uptake. The uptake of 0.4 micromol l-1of [3H]tyramine by rat liver slices was linear from 5 min up to the end of incubation. At 15 min the uptake was 4.58+/-0.18 pmol mg-1protein. The accumulation of [3H]tyramine was sensitive to temperature (69. 3+/-4.0% inhibition at 0 degrees C, P<0.001), to sodium omission replaced by 150 mmol l-1Tris or 110 mmol l-1Tris+40 mmol l-1choline (27.6+/-6.0%, P<0.01, and 24.6+/-3.8% inhibition, P<0.01, respectively), and the inhibition of Na+-K+-adenosine triphosphatase by 150 micromol l-1ouabain (20.4+/-2.6% decrease, P<0.01). Uptake of [3H]tyramine was cocaine- (10 micromol l-1) and desipramine- (1 micromol l-1) dependent (32.2+/-6.4%, P<0.05, and 31.6+/-4.0% inhibition, P<0.05, respectively). Uptake of [3H]tyramine in rat liver slices was not modified by 30 micromol l-1isoprenaline, 30 micromol l-1corticosterone, 30 micromol l-1normetanephrine and noradrenaline up to 4 micrometers at higher noradrenaline concentrations tyramine transport was diminished (P<0.05). Results achieved by incubation with increasing tyramine concentrations indicate that at the micromolar level hepatic uptake occurs by a combined passive diffusion and transport-mediated mechanism, whereas at greater tyramine 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.
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