Metabolic fate of glucose in vascular smooth muscle during contraction induced by norepinephrine

被引:28
作者
Barron, JT
Barany, M
Gu, LP
Parrillo, JE
机构
[1] Rush Presbyterian St Lukes Med Ctr, Dept Med, Cardiol Sect, Chicago, IL 60612 USA
[2] Univ Illinois, Coll Med, Dept Biochem, Chicago, IL 60612 USA
关键词
glucose oxidation; glycogen; glycolysis; lactic acid; muscle contraction; norepinephrine;
D O I
10.1006/jmcc.1997.0637
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
The metabolism of glucose in porcine carotid artery was tracked by isotopic methods during sustained isometric contraction induced by 100 mu M norepinephrine (NE). In resting muscles, 74 and 18% of glucose taken up was accounted for by glycolysis and glycogen synthesis, respectively. Lactate production accounted for 69%, pyruvate production for 12%, and glucose oxidation accounted for 14% of glycolytic nux. The oxidation of glucose accounted for 57% of the consumption of O-2 and thus constituted the primary oxidative substrate. During contraction by NE, glucose-uptake declined modestly below the resting basal rate. Glycolysis of external glucose and Lactate production decreased and then increased with sustained contraction. Norepinephrine stimulated simultaneous glycogenolysis and glycogen synthesis, with net glycogen synthesis prevailing over 90 min of isometric contraction. Furthermore, NE modified the distribution of glucosyl units throughout the glycogen pool. The steady state rate of oxidation of glucose did not increase during NE contraction, even though O-2-consumption increased. In contrast, increased glucose oxidation was demonstrable during contraction induced by 80 mM KCl. Furthermore, oxidation of exogenous fatty acid could be demonstrated during NE-induced contraction. Thus, NE exerts multiple effects on glucose and glycogen metabolism in smooth muscle, but it does not stimulate glucose oxidation. (C) 1998 Academic Press Limited.
引用
收藏
页码:709 / 719
页数:11
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