The microdialysis technique was used to study the effects of adrenergic agonists on the release of amino acids from rat skeletal muscle. The release was monitored indirectly by measurements of interstitial concentrations. To distinguish metabolic from vasoactive effects, the adrenaline and isoprenaline results were compared with those of vasopressin, alpha-agonists and adenosine. As determined by the microdialysis ethanol technique, adrenaline, alpha-agonists and vasopressin induced vasoconstriction, whereas isoprenaline and adenosine induced vasodilatation. The lactate-to-pyruvate ratio increased fourfold with adrenaline (P < 0.001) and by 54% with isoprenaline (P < 0.05), whereas no change was observed with alpha-agonists and adenosine. Vasopressin induced a fivefold increase in the lactate-to-pyruvate ratio (P < 0.001), but with an unchanged pyruvate concentration, indicating that the effect may have been secondary to ischaemia. Adrenaline induced a twofold and vasopressin a 34% increase in the concentration of alanine (P < 0.001), whereas isoprenaline, adenosine and alpha-agonists had no significant effect. Adrenaline-perfusion induced an initial anabolic effect as evidenced by a reduced concentration of tyrosine. A significant decrease in the glutamate-to-glutamine ratio was observed with adrenaline and isoprenaline (22 and 27%, P < 0.01) whereas alpha-agonists, vasopressin and adenosine were without effect. In conclusion, the present study showed that adrenaline, via a beta-adrenergically mediated activation of glycogenolysis, possibly further stimulated by ischaemia, induced an increased release of alanine from skeletal muscle. The study indicates a beta-adrenergic stimulation on the glutamine synthetase step and a short lasting anabolic effect of adrenaline. Differences in the magnitude of the effects of adrenaline and isoprenaline could be related to their different vasoactive properties.