Nitric oxide contributes to the augmented vasodilatation during hypoxic exercise
Nitric oxide contributes to the augmented vasodilatation during hypoxic exercise
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DOI：
10.1113/jphysiol.2009.180489
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发表时间：
2010-01-15
影响因子：
5.5
通讯作者：
Joyner, Michael J.
中科院分区：
文献类型：
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作者：
Casey, Darren P.;Madery, Brandon D.;Joyner, Michael J.
我们验证了以下假设：(1)缺氧运动时一氧化氮（NO）有助于增强骨骼肌血管舒张；(2)联合抑制NO的产生和腺苷受体的激活比单独抑制NO更能减弱缺氧运动时增强的血管舒张。在不同的方案中，受试者在常氧和常capnic缺氧（80%动脉O-2饱和度）时进行前臂运动（最大运动量的10%和20%）。在方案1 （n = 12）中，受试者接受动脉内给药生理盐水（对照组）和NO合成酶抑制剂n - g -单甲基- l-精氨酸（L-NMMA）。在方案2 （n = 10）中，受试者接受动脉盐水（对照组）和l- nmma -氨茶碱（腺苷受体拮抗剂）联合给药。根据前臂血流量（ml min(-1)）和血压（mmHg）计算前臂血管导度(FVC; ml min(-1) （100 mmHg)(-1)）。在方案1中，与生理盐水相比，L-NMMA在静息条件下和低氧运动期间由于缺氧引起的FVC（从低氧基线开始的δ）的变化显著降低（P < 0.01）。在方案2中，与生理盐水相比，联合使用l - nmma -氨茶碱降低了缺氧运动引起的δ FVC （P < 0.01）。然而，与相应的对照（生理盐水）条件相比，仅l-NMMA（方案1）和l-NMMA -氨茶碱联合（方案2）在10% （-17.5 +/- 3.7 vs -21.4 +/- 5.2%, P = 0.28）和20% （-13.4 +/- 3.5 vs -18.8 +/- 4.5%, P = 0.18）的低氧运动中δ FVC的相对减少相似。这些发现表明，一氧化氮有助于在缺氧运动中观察到的独立于腺苷的血管舒张增强。
We tested the hypotheses that (1) nitric oxide (NO) contributes to augmented skeletal muscle vasodilatation during hypoxic exercise and (2) the combined inhibition of NO production and adenosine receptor activation would attenuate the augmented vasodilatation during hypoxic exercise more than NO inhibition alone. In separate protocols subjects performed forearm exercise (10% and 20% of maximum) during normoxia and normocapnic hypoxia (80% arterial O-2 saturation). In protocol 1 (n = 12), subjects received intra-arterial administration of saline (control) and the NO synthase inhibitor N-G-monomethyl-L-arginine (L-NMMA). In protocol 2 (n = 10), subjects received intra-arterial saline (control) and combined l-NMMA-aminophylline (adenosine receptor antagonist) administration. Forearm vascular conductance (FVC; ml min(-1) (100 mmHg)(-1)) was calculated from forearm blood flow (ml min(-1)) and blood pressure (mmHg). In protocol 1, the change in FVC (Delta from normoxic baseline) due to hypoxia under resting conditions and during hypoxic exercise was substantially lower with L-NMMA administration compared to saline (control; P < 0.01). In protocol 2, administration of combined L-NMMA-aminophylline reduced the Delta FVC due to hypoxic exercise compared to saline (control; P < 0.01). However, the relative reduction in Delta FVC compared to the respective control (saline) conditions was similar between l-NMMA only (protocol 1) and combined L-NMMA-aminophylline (protocol 2) at 10% (-17.5 +/- 3.7 vs. -21.4 +/- 5.2%; P = 0.28) and 20% (-13.4 +/- 3.5 vs. -18.8 +/- 4.5%; P = 0.18) hypoxic exercise. These findings suggest that NO contributes to the augmented vasodilatation observed during hypoxic exercise independent of adenosine.