α₁, α₂-and β-Adrenoceptor densities and catecholamine responsiveness in established hepatoma cells, rat ascites hepatoma AH13, AH66, AH66F, AH109A, AH130 and AH7974 cells and human hepatocellular carcinoma HLF and HepG2 cells, were compared with those in normal rat hepatocytes and Chang liver cells. α₁-Adrenoceptor densities measured by [³H] prazosin bindings were not detected in all hepatoma cell lines. α₂-Adrenoceptor densities measured by [³H] clonidine bindings were also barely detected in hepatoma cell lines except for AH130 cells and HepG2 cells. Regarding β-adrenoceptor, AH109A, AH130 and AH7974 cells had much more [¹²⁵I] iodocyanopindolol binding sites than normal rat hepatocytes, although we could not detect the binding in HepG2 cells. Adenylate cyclase of normal rat hepatocyte and Chang liver cells were stimulated by β₂-adrenergic agonist salbutamol, while the cyclase in hepatoma cells had no β₂-adrenergic response but a β₁-type response. These findings indicate that the characteristics of adrenergic response in hepatoma cell lines is very different from that in normal hepatocytes, suggesting a participation in the hepatocarcinogenesis and/or the autonomous proliferation of hepatoma cells.