Nakata R, Tsukamoto I, Nanme M, Makino S, Miyoshi M, Kojo S
Eur J Pharmacol. 1985 Aug 27;114(3):355-60. doi: 10.1016/0014-2999(85)90380-2.
The increases in activity of hepatic thymidylate synthetase and of thymidine kinase, which catalyze the formation of thymidylate via the de novo and salvage pathways, respectively, were significantly suppressed during liver regeneration in rats which had been given alpha-adrenoceptor antagonists (phenoxybenzamine and phentolamine) or adrenergic neuron blockers (guanethidine and reserpine). These suppressions were not observed with a beta-adrenoceptor antagonist (propranolol), or an anticholinergic agent (atropine methyl nitrate). The rise in the activity of the thymidylate-synthesizing enzymes was closely correlated with the increase in the DNA content of the liver. It is concluded that catecholamine regulates the increase in the activity of thymidylate synthetase and thymidine kinase, which are key enzymes in DNA synthesis in regenerating liver. It is also suggested that sympathetic nerves play an important role in liver regeneration.
在给大鼠注射α-肾上腺素能受体拮抗剂（酚苄明和酚妥拉明）或肾上腺素能神经阻滞剂（胍乙啶和利血平）后，肝再生过程中催化通过从头合成途径和补救途径形成胸苷酸的肝胸苷酸合成酶和胸苷激酶的活性增加受到显著抑制。而β-肾上腺素能受体拮抗剂（普萘洛尔）或抗胆碱能药物（硝酸甲基阿托品）则未观察到这种抑制作用。胸苷酸合成酶活性的升高与肝脏DNA含量的增加密切相关。由此得出结论，儿茶酚胺调节胸苷酸合成酶和胸苷激酶活性的增加，这两种酶是再生肝脏中DNA合成的关键酶。还表明交感神经在肝脏再生中起重要作用。
