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首页> 外文期刊>American Journal of Physiology >Pentose phosphate pathway coordinates multiple redox-controlled relaxing mechanisms in bovine coronary arteries.
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Pentose phosphate pathway coordinates multiple redox-controlled relaxing mechanisms in bovine coronary arteries.

机译：磷酸戊糖途径可协调牛冠状动脉中多种氧化还原控制的放松机制。

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摘要

Pentose phosphate pathway (PPP) inhibitors, 6-aminonicotinamide (6-AN) and epiandrosterone (Epi), were employed to examine whether changes in NADP(H) redox regulates contractile force in endothelium-removed bovine coronary arteries (BCAs). 6-AN (0.01-5 mM) or Epi (1-500 microM) elicited dose-dependent relaxation in BCAs contracted with 30 mM KCl, 0.1 microM U-44619, and endothelin-1 but not with phorbol 12,13-dibutyrate, a protein kinase C activator that causes Ca2+-independent contraction. Relaxation to PPP inhibition was associated with oxidation of NADPH and glutathione (GSH). Relaxation to 6-AN was not mediated by H2O2, because it was not altered by hypoxia or the peroxide scavenger ebselen (100 microM). The thiol reductant DTT (3 mM) attenuated the relaxation to 6-AN and Epi by 30-40%. Inhibition of glycolysis or mitochondrial electron transport did not elicit relaxation in BCAs contracted with 30 mM KCl, suggesting these pathways may not be involved in relaxation elicited by PPP inhibition. High doses of K+ channel blockers [e.g., TEA (10 mM) and 4-aminopyridine (10 mM)] only partially inhibited the relaxation to 6-AN. On the basis of changes in the fura-2 fluorescence ratio, 6-AN and Epi appeared to markedly reduce intracellular Ca2+. Thus PPP inhibition oxidizes NADPH and GSH and appears to activate a novel coordination of redox-controlled relaxing mechanisms in BCAs mediated primarily through decreasing intracellular Ca2+.
机译：磷酸戊糖途径（PPP）抑制剂6-氨基烟酰胺（6-AN）和表雄甾酮（Epi）被用于检查NADP（H）氧化还原的变化是否调节内皮去除的牛冠状动脉（BCA）的收缩力。 6-AN（0.01-5 mM）或Epi（1-500 microM）引起BCA与30 mM KCl，0.1 microM U-44619和内皮素1收缩但不与佛波12,13-dibutyrate发生剂量依赖性舒张，一种蛋白激酶C激活剂，可引起不依赖Ca2 +的收缩。放松对PPP的抑制作用与NADPH和谷胱甘肽（GSH）的氧化有关。过氧化氢不会介导6-AN的松弛，因为它不会因缺氧或过氧化物清除剂依布硒仑（100 microM）而改变。硫醇还原剂DTT（3 mM）使松弛到6-AN和Epi降低了30-40％。糖酵解或线粒体电子转运的抑制并未引起与30 mM KCl接触的BCA的松弛，这表明这些途径可能不参与PPP抑制引起的松弛。高剂量的K +通道阻滞剂[例如TEA（10 mM）和4-氨基吡啶（10 mM）]仅部分抑制了6-AN的松弛。根据fura-2荧光比率的变化，6-AN和Epi似乎显着降低了细胞内Ca2 +。因此，PPP抑制作用会氧化NADPH和GSH，并似乎激活主要通过降低细胞内Ca2 +介导的BCA中氧化还原控制的松弛机制的新型配位。

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