Frucht H, Lilling G, Beitner R
Int J Biochem. 1984;16(4):397-402. doi: 10.1016/0020-711x(84)90138-1.
The intracellular concentration of glucose-1,6-bisphosphate (Glc-1,6-P2) in rat tibialis anterior muscle was markedly decreased following the injection of bradykinin. Injection of bradykinin also induced a significant increase in the level of cyclic GMP in muscle. The activity of glucose-1,6-bisphosphatase, the enzyme that degrades Glc-1,6-P2, was markedly enhanced by bradykinin, which may account for the decrease in the level of Glc-1,6-P2. The decrease in Glc-1,6-P2, the potent activator of phosphofructokinase and phosphoglucomutase, was accompanied by a concomitant reduction in these enzymes' activities. The bradykinin-induced decrease in Glc-1,6-P2 and in the activity of phosphofructokinase, the rate-limiting enzyme in glycolysis, may be involved in the pathogenic influences of this hormone in various clinical conditions.
注射缓激肽后,大鼠胫前肌中葡萄糖-1,6-二磷酸(Glc-1,6-P2)的细胞内浓度显著降低。注射缓激肽还导致肌肉中环鸟苷酸(cGMP)水平显著升高。缓激肽可显著增强降解Glc-1,6-P2的葡萄糖-1,6-二磷酸酶的活性,这可能是Glc-1,6-P2水平降低的原因。Glc-1,6-P2是磷酸果糖激酶和磷酸葡萄糖变位酶的强效激活剂,其水平降低伴随着这些酶活性的相应降低。缓激肽诱导的Glc-1,6-P2减少以及糖酵解限速酶磷酸果糖激酶活性降低,可能与该激素在各种临床病症中的致病作用有关。