Metcalfe A M, Phillips P, Dixon R M, Radda G K
MRC Clinical and Biochemical Resonance Unit, Department of Biochemistry, University of Oxford, UK.
J Mol Endocrinol. 1997 Apr;18(2):161-6. doi: 10.1677/jme.0.0180161.
Liver regeneration is significantly impaired in rats with both alpha-adrenergic hepatic denervation and hereditary vasopressin deficiency. This may implicate a direct role for these agonists in the process of compensatory hyperplasia. The mitogenic capacities of norepinephrine, vasopressin and hepatocyte growth factor (HGF), either alone or in combination were investigated by [3H]thymidine incorporation into hepatocyte cultures prepared from normal and regenerating rat livers. The results show that normal hepatocytes incorporate less [3H]thymidine in response to HGF than do regenerating hepatocytes. In addition, physiological concentrations of vasopressin cause a synergistic stimulation of [3H]thymidine uptake in rat liver cells in the presence of HGF.
在同时存在α-肾上腺素能肝去神经支配和遗传性血管加压素缺乏的大鼠中,肝脏再生明显受损。这可能意味着这些激动剂在代偿性增生过程中具有直接作用。通过将[3H]胸腺嘧啶核苷掺入从正常和再生大鼠肝脏制备的肝细胞培养物中,研究了去甲肾上腺素、血管加压素和肝细胞生长因子(HGF)单独或联合使用时的促有丝分裂能力。结果表明,与再生肝细胞相比,正常肝细胞对HGF的反应中掺入的[3H]胸腺嘧啶核苷较少。此外,在存在HGF的情况下,生理浓度的血管加压素会对大鼠肝细胞中[3H]胸腺嘧啶核苷的摄取产生协同刺激作用。