Keppens S, De Wulf H
Biochem J. 1984 Aug 15;222(1):277-80. doi: 10.1042/bj2220277.
Vasopressin and angiotensin are able to lower the glucagon-induced increase of cyclic AMP levels in isolated hepatocytes. Results presented are in favour of an enhanced phosphodiesterase activity to account for this cyclic AMP lowering effect. In particular, vasopressin prevents exogenous cyclic AMP from activating glycogen phosphorylase: in the presence of phosphodiesterase inhibitors, the hormone becomes unable to decrease glucagon-induced cyclic AMP levels. This anti-glucagon effect of vasopressin and angiotensin might be physiologically more important than their glycogenolytic effect; indeed, the latter is very transient in nature and, in addition, requires higher hormone concentrations [Bréant, Keppens & De Wulf (1981) Biochem. J. 200, 509-514] than those needed for the anti-glucagon effect, as reported here.
血管加压素和血管紧张素能够降低胰高血糖素诱导的离体肝细胞中环磷酸腺苷(cAMP)水平的升高。所呈现的结果支持磷酸二酯酶活性增强是造成这种cAMP水平降低效应的原因。特别是,血管加压素可阻止外源性cAMP激活糖原磷酸化酶:在磷酸二酯酶抑制剂存在的情况下,该激素无法降低胰高血糖素诱导的cAMP水平。血管加压素和血管紧张素的这种抗胰高血糖素作用在生理上可能比它们的糖原分解作用更重要;实际上,后者本质上非常短暂,此外,与本文报道的抗胰高血糖素作用相比,需要更高的激素浓度[Bréant、Keppens和De Wulf(1981年)《生物化学杂志》200, 509 - 514]。