Differential control by arterial and portal noradrenaline of hepatic carbohydrate metabolism: evidence for an indirect hemodynamic mechanism.

In an earlier study it was found (a) that arterial noradrenaline caused increases in glucose and lactate output slower in onset, smaller in peak height and clearly longer in duration than those caused by portal noradrenaline and (b) that arterial noradrenaline was extracted to a much greater extent than portal noradrenaline. It is possible that the differences in the actions of arterial and portal noradrenaline were due to the different hemodynamic changes; arterial noradrenaline reduced hepatic flow more strongly and with different kinetics than did portal noradrenaline. Therefore the effects of arterial and portal noradrenaline were investigated in isolated rat liver, single-pass perfused through both the hepatic artery (100 cm H2O, 30% flow) and the portal vein (15 cm H2O, 70% flow), after inhibition of the hemodynamic alterations by the Ca2+ antagonist nifedipine. We found (a) that nifedipine inhibited the hemodynamic changes by arterial noradrenaline strongly and those by portal noradrenaline slightly, (b) that the remaining hemodynamic alterations in the presence of high concentrations of the Ca2+ antagonist (100 mumol/L)--slight decrease in portal flow with unaffected arterial flow--were essentially identical after arterial and portal application of noradrenaline, (c) that the pronounced kinetic differences in the alterations by arterial and portal noradrenaline of glucose and lactate balance were diminished by 50 mumol/L nifedipine and abolished by 100 mumol/L of the Ca2+ antagonist and (d) that the different hepatic extractions of arterial and portal noradrenaline were greatly reduced and almost equalized by nifedipine.(ABSTRACT TRUNCATED AT 250 WORDS)