急性超氧化物清除可降低短期运动训练大鼠的交感血管收缩反应性。
Acute superoxide scavenging reduces sympathetic vasoconstrictor responsiveness in short-term exercise-trained rats.
机构信息
Faculty of Physical Education and Recreation, University of Alberta, Edmonton, Alberta, Canada.
出版信息
J Appl Physiol (1985). 2013 Jun;114(11):1511-8. doi: 10.1152/japplphysiol.00131.2013. Epub 2013 Apr 4.
We hypothesized that acute superoxide (O2(-)) scavenging would attenuate sympathetic vasoconstrictor responsiveness by augmenting nitric oxide (NO)-mediated inhibition of sympathetic vasoconstriction in exercise-trained rats. Sprague-Dawley rats were randomly assigned to sedentary time control (S; n = 7) or mild- (M: 20 m/min, 5° grade; n = 7) or heavy-intensity (H: 40 m/min, 5° grade; n = 7) exercise training (ET) groups and trained 5 days/wk for 4 wk with matched training volume. Following ET, rats were anesthetized and instrumented for lumbar sympathetic chain stimulation and measurement of femoral vascular conductance. In resting skeletal muscle, the percentage change of femoral vascular conductance in response to continuous (2 Hz) and patterned (20 and 40 Hz) sympathetic stimulation was determined during control conditions, O2(-) scavenging (TIRON, 1 g·kg(-1)·h(-1) iv) and combined O2(-) scavenging + nitric oxide synthase blockade (N(ω)-nitro-l-arginine methyl ester, 5 mg/kg iv). ET augmented the vasoconstrictor response to sympathetic stimulation in a training intensity-dependent manner (P < 0.05) (S: 2 Hz: -26 ± 7.1%; 20 Hz: -26.9 ± 7.3%; 40 Hz: -27.7 ± 7.0%; M: 2 Hz: -37.4 ± 8.3%; 20 Hz: -35.9 ± 7.4%; 40 Hz: -38.2 ± 9.4%; H: 2 Hz: -46.9 ± 7.8%; 20 Hz: -48.5 ± 7.2%; 40 Hz: -51.2 ± 7.3%). O2(-) scavenging did not alter (P > 0.05) the vasoconstrictor response in S rats (S: 2 Hz: -23.9 ± 7.6%; 20 Hz: -26.1 ± 9.1%; 40 Hz: -27.5 ± 7.2%), whereas the response in ET rats was diminished (M: 2 Hz: -26.3 ± 5.1%; 20 Hz: -28.7 ± 5.3%; 40 Hz: -28.5 ± 5.6%; H: 2 Hz: -35.5 ± 10.3%; 20 Hz: -38.6 ± 6.8%; 40 Hz: -43.9 ± 5.9%, P < 0.05). TIRON + N(ω)-nitro-l-arginine methyl ester increased vasoconstrictor responsiveness (P < 0.05) in ET rats (M: 2 Hz: -47.7 ± 9.8%; 20 Hz: -41.2 ± 7.2%; 40 Hz: -50.5 ± 7.9%; H: 2 Hz: -55.8 ± 7.6%; 20 Hz: -55.7 ± 7.8%; 40 Hz: -58.7 ± 6.2%), whereas, in S rats, the response was unchanged (2 Hz: -29.4 ± 8.7%; 20 Hz: -30.0 ± 7.4%; 40 Hz: -35.2 ± 10.3%; P > 0.05). These data indicate that the augmented sympathetic vasoconstrictor responsiveness in ET rats was related to increased oxidative stress and altered nitric oxide-mediated inhibition of vasoconstriction.
我们假设急性超氧化物（O2(-)）清除会通过增强一氧化氮（NO）介导的抑制交感神经血管收缩来减弱运动训练大鼠的交感血管收缩反应。随机将 Sprague-Dawley 大鼠分为安静时间对照（S；n = 7）或轻度（M：20 m/min，5°坡度；n = 7）或重度（H：40 m/min，5°坡度；n = 7）运动训练（ET）组，并在 4 周内每周 5 天进行匹配的训练量。ET 后，大鼠麻醉并进行腰交感神经链刺激和股血管导纳测量。在静息骨骼肌中，在对照条件下、超氧化物清除（TIRON，1 g·kg(-1)·h(-1)iv）和联合超氧化物清除+一氧化氮合酶阻断（N(ω)-硝基-l-精氨酸甲酯，5 mg/kg iv）期间，确定股血管导纳对连续（2 Hz）和模式（20 和 40 Hz）交感刺激的变化百分比。ET 以训练强度依赖的方式增强了对交感刺激的血管收缩反应（P < 0.05）（S：2 Hz：-26 ± 7.1%；20 Hz：-26.9 ± 7.3%；40 Hz：-27.7 ± 7.0%；M：2 Hz：-37.4 ± 8.3%；20 Hz：-35.9 ± 7.4%；40 Hz：-38.2 ± 9.4%；H：2 Hz：-46.9 ± 7.8%；20 Hz：-48.5 ± 7.2%；40 Hz：-51.2 ± 7.3%）。超氧化物清除（P > 0.05）没有改变 S 大鼠的血管收缩反应（S：2 Hz：-23.9 ± 7.6%；20 Hz：-26.1 ± 9.1%；40 Hz：-27.5 ± 7.2%），而 ET 大鼠的反应则减弱（M：2 Hz：-26.3 ± 5.1%；20 Hz：-28.7 ± 5.3%；40 Hz：-28.5 ± 5.6%；H：2 Hz：-35.5 ± 10.3%；20 Hz：-38.6 ± 6.8%；40 Hz：-43.9 ± 5.9%，P < 0.05）。TIRON + N(ω)-硝基-l-精氨酸甲酯增加了 ET 大鼠的血管收缩反应（P < 0.05）（M：2 Hz：-47.7 ± 9.8%；20 Hz：-41.2 ± 7.2%；40 Hz：-50.5 ± 7.9%；H：2 Hz：-55.8 ± 7.6%；20 Hz：-55.7 ± 7.8%；40 Hz：-58.7 ± 6.2%），而在 S 大鼠中，反应没有变化（2 Hz：-29.4 ± 8.7%；20 Hz：-30.0 ± 7.4%；40 Hz：-35.2 ± 10.3%；P > 0.05）。这些数据表明，ET 大鼠交感神经血管收缩反应增强与氧化应激增加和一氧化氮介导的血管收缩抑制改变有关。
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