Title of article :
Metabolic Fate of Glucose in Vascular Smooth Muscle During Contraction Induced by Norepinephrine
Author/Authors :
John T Barron، نويسنده , , Michael B?r?ny، نويسنده , , Liping Gu، نويسنده , , Joseph E Parrillo، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1998
Pages :
11
From page :
709
To page :
719
Abstract :
The metabolism of glucose in porcine carotid artery was tracked by isotopic methods during sustained isometric contraction induced by 100μmnorepinephrine (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 flux. The oxidation of glucose accounted for 57% of the consumption of O2and 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 O2-consumption increased. In contrast, increased glucose oxidation was demonstrable during contraction induced by 80 m 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.
Keywords :
glycogen , Glucose oxidation , glycolysis , Muscle Contraction , Norepinephrine. , Lactic acid
Journal title :
Journal of Molecular and Cellular Cardiology
Serial Year :
1998
Journal title :
Journal of Molecular and Cellular Cardiology
Record number :
525954
Link To Document :
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