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首页> 外文期刊>American Journal of Physiology >Opposing effects of coupled and uncoupled NOS activity on the Na+-K' pump in cardiac myocytes
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Opposing effects of coupled and uncoupled NOS activity on the Na+-K' pump in cardiac myocytes

机译：耦合和未耦合的NOS活性对心肌细胞Na + -K“泵的相反作用

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First published December 5, 2007; doi:10.1152/ajpcell.00242.2007.-Pharmacological delivery of nitric oxide (NO) stimulates the cardiac Na+-K+ pump. However, effects of NO synthesized by NO synthase (NOS) often differ from the effects of NO delivered pharmacologically. In addition, NOS can become "uncoupled" and preferentially synthesize O2_, which often has opposing effects to NO. We tested the hypothesis that NOS-synfhesized NO stimulates Na+-K+ pump activity, and uncoupling of NOS inhibits it. To image NO, we loaded isolated rabbit cardiac myocytes with 4,5-diaminofluorescein-2 diacetate (DAF-2 DA) and measured fluorescence with confocal microscopy. L-Arginine (L-Arg; 500 mumol/l) increased DAF-2 DA fluorescence by 51% compared with control (n - 8; P < 0.05). We used the whole cell patch-clamp technique to measure electrogenic Na~+-K~+ pump current (7P). Mean 7P of 0.35 +- 0.03 pA/pF (n = 44) was increased to 0.48 +- 0.03 pA/pF (n = 7, P < 0.05) by 10 mumol/l L-Arg in pipette solutions. This increasewas abolished by NOS inhibition with radicicol or by NO-activated guanylyl cyclase inhibition with lH-[l,2,4]oxadia-zole[4,3-a]quinoxalin-l-one. We next examined the effect of uncoupling NOS using paraquat. Paraquat (1 mmol/1) induced a 51% increase in the fluorescence intensity of O2~- sensitive dye dihydro-ethidium compared with control (n = 9; P < 0.05). To examine the functional effects of uncoupling, we measured 7P with 100 mumol/l paraquat included in patch pipette solutions. This decreased Ip to 0.28 +-0.03 pA/pF (n = 12; P < 0.001). The paraquat-induced pump inhibition was abolished by superoxide dismutase (in pipette solutions). We conclude that NOS-mediated NO synthesis stimulates the Na~+-K~+ pump, whereas uncoupling of NOS causes O2~--mediated pump inhibition.
机译：首次发布于2007年12月5日; doi：10.1152 / ajpcell.00242.2007.-一氧化氮（NO）的药理传递会刺激心脏Na + -K +泵。然而，由NO合酶（NOS）合成的NO的作用通常不同于药理上传递的NO的作用。此外，NOS可能会“解偶联”并优先合成O2_，这通常会与NO产生相反的影响。我们检验了NOS合成的NO刺激Na + -K +泵浦活性，而NOS的解偶联抑制它的假设。为了对NO成像，我们用4,5-二氨基荧光素2双乙酸盐（DAF-2 DA）加载了离体的兔心肌细胞，并用共聚焦显微镜测量了荧光。 L-精氨酸（L-Arg; 500μmol/ l）与对照相比（n-8; P <0.05）使DAF-2 DA荧光增加51％。我们使用全细胞膜片钳技术来测量电Na〜+ -K〜+泵浦电流（7P）。在移液器溶液中，通过10μmol/ l L-Arg，平均7P（0.35±0.03 pA / pF（n = 44））增加到0.48±0.03 pA / pF（n = 7，P <0.05）。这种增加被紫杉醇对NOS的抑制作用或对1H- [1,2,4]恶二唑-唑[4,3-a]喹喔啉-1-酮的NO激活的鸟嘌呤环化酶抑制作用所消除。接下来，我们研究了使用百草枯解耦NOS的效果。与对照组相比，百草枯（1 mmol / 1）诱导O2 +敏感染料二氢乙啶的荧光强度增加了51％（n = 9; P <0.05）。为了检查解偶联的功能效果，我们在贴片移液器溶液中用100μmol/ l百草枯测量了7P。这使Ip降低至0.28 + -0.03 pA / pF（n = 12; P <0.001）。百草枯引起的泵抑制作用被超氧化物歧化酶（在移液器中）消除了。我们得出的结论是，NOS介导的NO合成刺激Na〜+ -K〜+泵，而NOS的解偶联导致O2〜介导的泵抑制。

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