Constable S H, Favier R J, Uhl J, Holloszy J O
J Appl Physiol (1985). 1986 Sep;61(3):881-4. doi: 10.1152/jappl.1986.61.3.881.
The purpose of this study was to evaluate the report that bradykinin is the "muscle activity hypoglycemia factor" responsible for the activation of glucose transport that occurs in response to muscle contractile activity. Stimulation of rat epitrochlearis muscles to contract resulted in approximately a fourfold increase in the rate of intracellular accumulation of the nonmetabolizable glucose analog 3-O-methylglucose. Incubation of the muscles with high concentrations of aprotinin (Trasylol), a polypeptide inhibitor of kallikrein which blocks formation of kinins, did not inhibit the activation of sugar transport by contractile activity. Furthermore incubation of muscles with bradykinin did not have a stimulatory effect on the uptake of 3-methylglucose either at a physiological concentration or at high concentrations. These results provide no support for the claims that aprotinin prevents the activation of sugar transport in muscle by contractile activity or that bradykinin is the muscle activity hypoglycemia factor.
本研究的目的是评估缓激肽是“肌肉活动低血糖因子”这一报告，该因子负责激活因肌肉收缩活动而发生的葡萄糖转运。刺激大鼠肱三头肌收缩导致不可代谢的葡萄糖类似物3 - O - 甲基葡萄糖的细胞内积累速率增加约四倍。用高浓度抑肽酶（Trasylol）孵育肌肉，抑肽酶是一种激肽释放酶的多肽抑制剂，可阻断激肽的形成，但它并不抑制收缩活动对糖转运的激活。此外，用缓激肽孵育肌肉，无论是在生理浓度还是高浓度下，对3 - 甲基葡萄糖的摄取都没有刺激作用。这些结果不支持以下说法：抑肽酶可防止收缩活动激活肌肉中的糖转运，或者缓激肽是肌肉活动低血糖因子。
