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Cell-to-cell communication via gap junctions has been proposed to be involved in the metabolic actions of sympathetic liver nerves in the rat, The effects of hcpatic nerve stimulation and noradrenaline-, PGF> -and glucagon infusion on glucose metabolism and perfusion flow were studied in perfused rat liver in the absence and presence of the gap junctional inhibitors, hcptanol, carbenoxolonc and (4fi)phorbol 12myristate 13.acetate (4PPMA). (i) Stimulation of the hepatic nerve plexus increased glucose output, decreased flow and caused an overflow of noradrenaline into the hepatic vein. (ii) Heptanol completely inhibited not only the nerve stimulation-dependent metabolic and hemodynamic alterations but also the noradrenaline overflow. Thus the heptanol-dependent inhibitions were caused primarily by a strong impairment of transmitter release. (iii) Carbenoxolone inhibited the effects of ncurostimulation on glucose metabolism partially by about 50%. whereas it left perfusion flow and noradrenaline overflow essentially unaltered. (iv) 4bPMA reduced the nerve stimukdtion-dependent enhancement of glucose release by about 80% but the noradrenaline-dependent increase in glucose output only by about 30%; the increase in glucose release by PGF:. and by glumgon remained essentially unaltered, 4pPMA reduced the nerve stimulation-dependent decrease in portal flow by about 35% but did not affect the noradrenalincand PGFh-elicited alterations, nor did it alter noradrenaline overtlow. The results allow the conclusion that gap junctional communication plays a major role in the regulation of hepatic carbohydrate metabolism by sympathetic liver nerves, but not by circulating noradrenaline. PGF, or glucagon.