Andersson S M
Endocrinology. 1983 Feb;112(2):466-9. doi: 10.1210/endo-112-2-466.
Isoproterenol, phenylephrine, and salbutamol (all 100 microM) induced the activity of tyrosine aminotransferase (TAT; EC 2.6.1.5) by 109%, 72%, and 141%, respectively, in organ culture of fetal human liver. Propranolol (100 microM) inhibited the effects of isoproterenol and phenylephrine. In organ culture of fetal rat liver, the induction of TAT activity by phenylephrine (100 microM) was not significantly affected by phentolamine (100 microM), whereas it was abolished by a combination of phentolamine and propranolol (both 100 microM). Isoproterenol and salbutamol caused significant increases in TAT activity, which were not affected by 100 microM atenolol but were completely inhibited by propranolol (100 microM). The results show that the fetal human liver has developed responsiveness to adrenergic stimuli at the 12th week of gestation. The adrenergic induction of TAT in fetal human liver is mediated solely by beta-adrenergic mechanisms. In the fetal rat liver, the adrenergic induction of TAT is mediated by beta 2-adrenergic receptors.
在人胎儿肝脏器官培养中，异丙肾上腺素、去氧肾上腺素和沙丁胺醇（均为100微摩尔）分别使酪氨酸转氨酶（TAT；EC 2.6.1.5）的活性提高了109%、72%和141%。普萘洛尔（100微摩尔）抑制了异丙肾上腺素和去氧肾上腺素的作用。在胎鼠肝脏器官培养中，去氧肾上腺素（100微摩尔）对TAT活性的诱导作用不受酚妥拉明（100微摩尔）的显著影响，而酚妥拉明和普萘洛尔（均为100微摩尔）联合使用则消除了这种诱导作用。异丙肾上腺素和沙丁胺醇使TAT活性显著增加，这不受100微摩尔阿替洛尔的影响，但被普萘洛尔（100微摩尔）完全抑制。结果表明，人胎儿肝脏在妊娠第12周时已对肾上腺素能刺激产生反应。人胎儿肝脏中TAT的肾上腺素能诱导仅由β-肾上腺素能机制介导。在胎鼠肝脏中，TAT的肾上腺素能诱导由β2-肾上腺素能受体介导。
