Metabolic events stimulated by epinephrine and norepinephrine in hepatocytes isolated from fetal and early postnatal male rats are largely mediated through the P,-adrenergic receptor-/cyclic AMP dependent-system, whereas the same stimuli are transduced through the a, -adrenergic receptor-iphosphatidylinositol dependent-system in hepatocytes isolated from young adult male rats. This developmental transition was investigated by correlating hepatic a,-and p,-adrenergic receptor gene transcript levels with receptor levels as determined with selective radioligands in livers from late fetal to postnatal day 120 male Sprague-Dawley rats. P,-Adrenergic receptor concentration, initially high in membrane preparations isolated from fetal livers (203 i 21 fmolimg protein), dropped precipitously in postnatal day 6 livers (14 k 2 fmol/mg protein) and remained low throughout development out to postnatal day 90. P,-Adrenergic receptor mRNA levels were highest in fetal livers, weredecreased somewhat in postnatal day 6 livers and were undetectable in livers beyond postnatal day 15. In contrast, hepatic a,-adrenergic receptor concentration was relatively low in fetal livers (86 ? 25 fmolirng protein) and remained low until postnatal day 18. Thereafter, a steady increase in a,-adrenergic receptors was observed until adult levels. (270 2 24 fmolirng protein) were achieved at postnatal day 27. a,-Adrenergic receptor mRNA levels increased -3-fold, reaching a peak at postnatal day 24. Surprisingly, at postnatal day 30 hepatic a,-adrenergic receptor mRNA levels dropped to fetal levels; but, gradually increased with continued development. Thus, hepatic a,-and PLadrenergic receptors appear to be under complex regulatory control which may include transcriptional, as well as post-transcriptional, mechanisms.