Steiner K E, Stevenson R W, Green D R, Cherrington A D
Metabolism. 1985 Nov;34(11):1020-3. doi: 10.1016/0026-0495(85)90073-3.
Epinephrine (10(-7) mol/L) addition to isolated canine hepatocytes activates glycogen phosphorylase from 12.3 +/- 0.4 to 28.6 +/- 2.6 U/g and glucose output from 42 +/- 3 to 170 +/- 24 nmol/mg/h. Preincubation of hepatocytes with propranolol (2 X 10(-5) mol/L) caused a 73% inhibition of phosphorylase activation and a 77% inhibition of the stimulation of glucose output by epinephrine. Phentolamine (2 X 10(-5) mol/L) on the other hand, caused a 16% inhibition of phosphorylase activation and a 27% inhibition of the stimulation of glucose output by epinephrine. These results were unaffected by the sex of the animal. In the dog the glycogenolytic effects of epinephrine appear to be mediated primarily by a beta-adrenergic mechanism.
向分离的犬肝细胞中添加肾上腺素（10⁻⁷摩尔/升）可使糖原磷酸化酶活性从12.3±0.4单位/克激活至28.6±2.6单位/克，葡萄糖输出量从42±3纳摩尔/毫克/小时增加至170±24纳摩尔/毫克/小时。用普萘洛尔（2×10⁻⁵摩尔/升）对肝细胞进行预孵育，可使磷酸化酶激活受到73%的抑制，肾上腺素对葡萄糖输出的刺激作用受到77%的抑制。另一方面，酚妥拉明（2×10⁻⁵摩尔/升）可使磷酸化酶激活受到16%的抑制，肾上腺素对葡萄糖输出的刺激作用受到27%的抑制。这些结果不受动物性别的影响。在犬类中，肾上腺素的糖原分解作用似乎主要由β-肾上腺素能机制介导。
