Control of glycogenolysis and blood flow by arterial and portal adrenaline in perfused liver

Abstract

In isolated liver from fed rats, simultaneously single-pass-perfused via both the hepatic artery (80 mmHg, 30-35% flow) and the portal vein (10 mmHg, 70-65% flow), adrenaline was infused either singly or jointly via the hepatic artery or the portal vein in the absence or presence of the alpha 1-blocker prazosin and the beta 2-blocker butoxamine. It was found that: (1) arterial adrenaline caused increases in glucose and lactate output which were slower in onset, smaller in peak height but longer in duration than did portal adrenaline; (2) arterial adrenaline elicited a much more pronounced decrease in flow and increase in pressure in the ipsilateral vessel than did portal adrenaline, and arterial, but not portal, adrenaline elicited qualitatively similar alterations also in the contralateral vessel; (3) arterial adrenaline caused metabolic changes mainly via alpha 1-receptors, with beta 2-receptors playing a permissive role via haemodynamic alterations, whereas portal adrenaline acted only via alpha 1-receptors; (4) arterial adrenaline decreased arterial flow via alpha 1-receptors counteracted via beta 2-receptors and operated on portal flow as portal adrenaline only via alpha 1-receptors; and (5) arterial adrenaline was extracted to a far greater extent than portal adrenaline. The results indicate that the hepatic artery and the portal vein can function as independent sites of hormonal signal input, which interact by complex, still undefined, mechanisms.