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血管平滑肌张力产生和维持过程中的糖原代谢。

Glycogen metabolism during tension generation and maintenance in vascular smooth muscle.

作者信息

Lynch R M, Kuettner C P, Paul R J

机构信息

Department of Physiology and Biophysics, College of Medicine, University of Cincinnati, Ohio 45267-0576.

出版信息

Am J Physiol. 1989 Oct;257(4 Pt 1):C736-42. doi: 10.1152/ajpcell.1989.257.4.C736.

DOI:10.1152/ajpcell.1989.257.4.C736
PMID:2801923
Abstract

To study the regulation of glycogen utilization in vascular smooth muscle, we measured the content of glycogen and glucose 6-phosphate and the activity of the glycogen phosphorylase and glycogen debrancher enzymes in porcine carotid artery. During active contraction, the rates of glycogen phosphorylase and glycogenolysis were as high as expected. Despite this, glycogen content did not decrease to less than approximately 50% of control levels even after sustained contractions. The activity of glycogen debrancher enzyme was found to be limiting glycogen utilization at this point. Although glycogenolysis is closely coordinated with increases in oxidative metabolism concomitant with active contraction, the maximal level of tension obtained after stimulation was not substantially reduced under conditions where glycogen debrancher enzyme was limiting glycogen utilization. On the other hand, the rate of tension generation was increased in these tissues. Thus glycogen utilization is not necessary for maximal force generation per se, but may influence other muscle contractile properties. Finally, during steady-state tension maintenance, glycogen utilization is likely to be regulated by the intracellular concentrations of metabolic intermediates (glucose, glucose 6-phosphate), as it is in skeletal muscle.

摘要

为研究血管平滑肌中糖原利用的调节机制,我们测定了猪颈动脉中糖原、6-磷酸葡萄糖的含量以及糖原磷酸化酶和糖原脱支酶的活性。在主动收缩过程中,糖原磷酸化酶和糖原分解的速率如预期般高。尽管如此,即使在持续收缩后,糖原含量也不会降至低于对照水平的约50%。此时发现糖原脱支酶的活性限制了糖原的利用。虽然糖原分解与主动收缩时氧化代谢的增加密切相关,但在糖原脱支酶限制糖原利用的条件下,刺激后获得的最大张力水平并未大幅降低。另一方面,这些组织中张力产生的速率增加。因此,糖原利用本身并非产生最大力量所必需,但可能会影响其他肌肉收缩特性。最后,在稳态张力维持期间,糖原利用可能如在骨骼肌中一样,受代谢中间产物(葡萄糖、6-磷酸葡萄糖)的细胞内浓度调节。

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