Electrical stimulation of perivascular nerves (20 Hz/2 ms/20 V) in perfused rat liver led to a transient increase of ¹⁴CO₂ production from [1‐¹⁴C]glutamate, glutathione and thiol efflux, an increase in the lactate/pyruvate and the 3‐hydroxybutyrate/acetoacetate ratio, glucose release and of portal pressure.

These metabolic effects were accompanied by a Ca²⁺ release from the liver within the initial 2 min, being followed by Ca²⁺ reuptake, which lasted about 3 min. The initial Ca²⁺ release was 67 nmol/g liver and was smaller than that observed after phenylephrine (5 μM) addition (156 nmol/g liver). Hepatic Ca²⁺ release following nerve stimulation or phenylephrine was not significantly affected when the hemodynamic changes were largely prevented by sodium nitroprusside (10 μM). Although the amounts of Ca²⁺ released were different, the glycogenolytic responses, but not the other metabolic effects, were quantitatively similar with nerve stimulation and phenylephrine.

Within the first 3 min of nerve stimulation there was a K⁺ uptake by the liver being followed by a K⁺ release over the next 5–6 min and a subsequent slow K⁺ uptake phase. These changes resembled those observed with phenylephrine. Phentolamine, an α‐adrenergic antagonist, abolished the Ca²⁺ and K⁺ movements following nerve stimulation as well as glucose release and the hemodynamic changes. During continuous infusion of phenylephrine, nerve stimulation led still to an increase of portal pressure; however, the effects of nerve stimulation on Ca²⁺ and K⁺ fluxes and glucose release were largely suppressed.

It is concluded that the metabolic effects of electrical nerve stimulation are mediated by a redistribution of cellular Ca²⁺ following α‐receptor activation. Nerve stimulation involves Ca²⁺ and K⁺ fluxes across the plasma membrane. The metabolic effects are qualitatively similar to those induced by phenylephrine. The quantitative difference between nerve stimulation and phenylephrine is explained by a differential subacinar response, with fewer cells being reached by nerve stimulation than cells containing α‐receptors. The hemodynamic changes of nerve stimulation point to the existence of sphincters near the inflow of the sinusoidal bed.