Adenosine stimulates glycolytic flux in isolated perfused rat hearts by A1-adenosine receptors.
Adenosine stimulates glycolytic flux in isolated perfused rat hearts by A1-adenosine receptors.
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腺苷通过 A1-腺苷受体刺激离体灌注大鼠心脏中的糖酵解通量。
DOI：
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发表时间：
1989
影响因子：
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通讯作者：
Robert M. Mentzer
中科院分区：
文献类型：
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作者：
D. A. Wyatt;M. Edmunds;R. Rubio;Robert M. Berne;R. Lasley;Robert M. Mentzer
本研究旨在评估腺苷在心肌利用外源性葡萄糖的调节中的作用。用含有D-[3- 3 H]葡萄糖的缓冲液灌注离体大鼠心脏，并分析冠状动脉流出物的3 H2O产生，作为糖酵解通量的指标。最初，在五种不同条件下测定糖酵解通量：1）常氧; 2）常氧加100 μ M腺苷; 3）常氧加100 μ M腺苷和10 μ M 8-（磺苯基）-茶碱（SPT），一种腺苷受体拮抗剂; 4）缺氧;和5）缺氧加10 μ M SPT。腺苷和缺氧都使糖酵解通量增加约三倍，而用SPT阻断腺苷受体则会减弱这种增加。接下来，在常氧条件下，用不同浓度的R-苯基异丙基腺苷（PIA）（A1-腺苷受体激动剂）或5 '-N-乙基羧酰胺腺苷（NECA）（A2-腺苷受体激动剂）灌注心脏。糖酵解通量的显着增加发生与PIA，而NECA治疗导致糖酵解通量只有一个边际刺激。这些数据提供的证据表明：1）外源性腺苷刺激糖酵解流量在常氧心肌; 2）内源性腺苷刺激糖酵解流量在缺氧期间;和3）腺苷对糖酵解流量的影响是通过与A1-腺苷受体的相互作用介导的。
This study was designed to assess the role of adenosine in the regulation of exogenous glucose utilization by myocardium. Perfusion of isolated rat hearts with buffer containing D-[3-3H]glucose and analysis of the coronary effluent for 3H2O production was used as an indicator of glycolytic flux. Initially, glycolytic flux was determined during five different conditions: 1) normoxia; 2) normoxia plus 100 microM adenosine; 3) normoxia plus 100 microM adenosine and 10 microM 8-(sulfophenyl)-theophylline (SPT), an adenosine receptor antagonist; 4) hypoxia; and 5) hypoxia plus 10 microM SPT. Both adenosine and hypoxia produced an approximate threefold increase in glycolytic flux that was attenuated by adenosine receptor blockade with SPT. Next, hearts were perfused during normoxic conditions with various concentrations of either R-phenylisopropyladenosine (PIA), an A1-adenosine receptor agonist, or 5'-N-ethylcarboxamidoadenosine (NECA), an A2-adenosine receptor agonist. Significant increases in glycolytic flux occurred with PIA, whereas NECA treatment resulted in only a marginal stimulation of glycolytic flux. These data provide evidence that: 1) exogenous adenosine stimulated glycolytic flux in the normoxic myocardium; 2) endogenous adenosine stimulated glycolytic flux during hypoxia; and 3) the effect of adenosine on glycolytic flux was mediated by interaction with A1-adenosine receptors.