Just Timothy P, Jendzjowsky Nicholas G, DeLorey Darren S
Faculty of Physical Education and Recreation, University of Alberta, Edmonton, Alberta, Canada, T6G 2H9.
J Physiol. 2015 May 1;593(9):2213-24. doi: 10.1113/JP270279. Epub 2015 Mar 31.
Physical inactivity increases the risk of cardiovascular disease and may alter sympathetic nervous system control of vascular resistance. Hindlimb unweighting (HU), a rodent model of physical inactivity, has been shown to diminish sympathetic vasoconstrictor responsiveness and reduce NO synthase expression in isolated skeletal muscle blood vessels. Our understanding of the effects of HU on sympathetic vascular regulation in vivo is very limited. The present findings demonstrate that HU did not alter sympathetic vasoconstrictor responsiveness and NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle. This study suggests that short-term physical inactivity does not alter in vivo sympathetic vascular control in the skeletal muscle vascular bed at rest and during contraction.
We tested the hypothesis that physical inactivity would increase sympathetic vasoconstrictor responsiveness and diminish NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle. Sprague-Dawley rats (n = 33) were randomly assigned to sedentary time control (S) or hindlimb unweighted (HU) groups for 21 days. Following the intervention, rats were anaesthetized and instrumented for measurement of arterial blood pressure and femoral artery blood flow and stimulation of the lumbar sympathetic chain. The percentage change of femoral vascular conductance (%FVC) in response to sympathetic chain stimulation delivered at 2 and 5 Hz was determined at rest and during triceps surae muscle contraction before (control) and after NO synthase blockade with l-NAME (5 mg kg i.v.). Sympathetic vasoconstrictor responsiveness was not different (P > 0.05) in S and HU rats at rest (S, 2 Hz, -26 ± 8% and 5 Hz, -46 ± 12%; and HU, 2 Hz, -29 ± 9% and 5 Hz, -51 ± 10%) and during contraction (S, 2 Hz, -10 ± 7% and 5 Hz, -23 ± 11%; and HU, 2 Hz, -9 ± 5% and 5 Hz, -22 ± 7%). Nitric oxide synthase blockade caused a similar increase (P > 0.05) in sympathetic vasoconstrictor responsiveness in HU and S rats at rest (S, 2 Hz, -41 ± 7% and 5 Hz, -58 ± 8%; and HU, 2 Hz, -43 ± 6% and 5 Hz, -63 ± 8%) and during muscle contraction (S, 2 Hz, -15 ± 6% and 5 Hz, -31 ± 11%; and HU, 2 Hz, -12 ± 5% and 5 Hz, -29 ± 8%). Skeletal muscle NO synthase expression and ACh-mediated vasodilatation were also not different between HU and S rats. These data suggest that HU does not alter sympathetic vasoconstrictor responsiveness and NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle.
缺乏身体活动会增加心血管疾病风险，并可能改变交感神经系统对血管阻力的控制。后肢去负荷（HU）是一种缺乏身体活动的啮齿动物模型，已被证明会降低交感缩血管反应性，并减少分离的骨骼肌血管中一氧化氮合酶的表达。我们对HU在体内对交感神经血管调节作用的了解非常有限。目前的研究结果表明，HU不会改变静息和收缩骨骼肌中的交感缩血管反应性以及一氧化氮介导的对交感缩血管作用的抑制。这项研究表明，短期缺乏身体活动不会改变静息和收缩状态下骨骼肌血管床的体内交感神经血管控制。
我们检验了以下假设：缺乏身体活动会增加交感缩血管反应性，并减少静息和收缩骨骼肌中一氧化氮介导的对交感缩血管作用的抑制。将33只Sprague-Dawley大鼠随机分为久坐时间对照组（S）或后肢去负荷组（HU），为期21天。干预后，将大鼠麻醉并安装仪器以测量动脉血压和股动脉血流量，并刺激腰交感神经链。在静息状态和比目鱼肌收缩期间，在使用L-NAME（5mg/kg静脉注射）阻断一氧化氮合酶之前（对照）和之后，测定2Hz和5Hz刺激腰交感神经链时股血管传导率（%FVC）的变化百分比。在静息状态下（S组，2Hz时为-26±8%，5Hz时为-46±12%；HU组，2Hz时为-29±9%，5Hz时为-51±10%）和收缩期间（S组，2Hz时为-10±7%，5Hz时为-23±11%；HU组，2Hz时为-9±5%，5Hz时为-22±7%），S组和HU组大鼠的交感缩血管反应性无差异（P>0.05）。一氧化氮合酶阻断在静息状态下（S组，2Hz时为-41±7%，5Hz时为-58±8%；HU组，2Hz时为-43±6%，5Hz时为-63±8%）和肌肉收缩期间（S组，2Hz时为-15±6%，5Hz时为-31±11%；HU组，2Hz时为-12±5%，5Hz时为-29±8%），使HU组和S组大鼠的交感缩血管反应性有相似的增加（P>0.05）。HU组和S组大鼠的骨骼肌一氧化氮合酶表达和乙酰胆碱介导血管舒张也无差异。这些数据表明，HU不会改变静息和收缩骨骼肌中的交感缩血管反应性以及一氧化氮介导的对交感缩血管作用的抑制。
