Sex differences in sympathetic vasoconstrictor responsiveness and sympatholysis
Sex differences in sympathetic vasoconstrictor responsiveness and sympatholysis
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DOI：
10.1152/japplphysiol.00139.2017
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发表时间：
2017-07-01
影响因子：
3.3
通讯作者：
DeLorey, Darren S.
中科院分区：
文献类型：
--
作者：
Just, Timothy P.;DeLorey, Darren S.
据报道，血压和血管阻力的神经血管控制存在性别差异。然而，性别调节影响的机制尚未完全阐明。一氧化氮 (NO) 已被证明可以抑制静止和收缩骨骼肌中的交感血管收缩，雌激素可调节一氧化氮合酶 (NOS) 的表达和一氧化氮的生物利用度。因此，NO 介导的交感血管收缩抑制作用在女性中可能会增强。因此，本研究的目的是调查以下假设：与男性相比，女性交感血管收缩反应性会减弱，NO 介导的交感血管收缩抑制会增强。将雄性（M；n = 8）和雌性（F；n = 10）Sprague-Dawley 大鼠麻醉并通过外科手术测量动脉血压和股动脉血流量并刺激腰交感链。在 NOS 阻断之前（对照）和之后，在休息时和小腿三头肌收缩期间测定股骨血管电导响应于 2 和 5 Hz 交感链刺激的百分比变化[N-omega-硝基-L-精氨酸甲酯（L-NAME），10 mg/kg iv]。静息时，2 Hz 频率下雌性大鼠的交感血管收缩反应性比雄性大鼠增强 (P < 0.05) [F: -33 +/- 8% (SD)； M：-26 +/- 6%]，但在 5 Hz 时没有差异（F：-55 +/- 7%；M：-47 +/- 7%）。在肌肉收缩过程中，2 Hz 频率下女性和男性诱发的血管收缩相似 (P < 0.05)（F：-12 +/- 5%；M：-13 +/- 5%），但与男性相比，5 Hz 频率下女性诱发的血管收缩减弱（P < 0.05）（F：-24 +/- 5%；M：-34 +/- 8%）。 L-NAME 增加了两组在休息和收缩期间的交感血管收缩反应性（P < 0.05）。与男性相比，女性中收缩介导的血管收缩（交感神经松解）抑制作用增强（P < 0.05）；然而，在 NOS 阻断的情况下，雄性和雌性之间的交感作用没有差异（P < 0.05），这表明雌性大鼠中 NO 介导的交感作用增强。这些数据表明，性别调节静止和收缩骨骼肌中的交感血管控制，并且雌性大鼠中增强的交感神经的一部分是不依赖的。新的和值得注意的血压和血管阻力的神经血管调节的性别差异已被记录。然而，我们对调节这些差异的根本机制的理解并不完整。本研究表明，雌性大鼠在运动过程中抑制交感血管收缩（交感神经溶解）的能力增强，并且一氧化氮介导部分增强的交感神经收缩。
Sex differences in the neurovascular control of blood pressure and vascular resistance have been reported. However, the mechanisms underlying the modulatory influence of sex have not been fully elucidated. Nitric oxide (NO) has been shown to inhibit sympathetic vasoconstriction in resting and contracting skeletal muscle, and estrogen modulates NO synthase (NOS) expression and NO bioavailability. Therefore NO-mediated inhibition of sympathetic vasoconstriction may be enhanced in females. Thus the purpose of the present study was to investigate the hypothesis that sympathetic vasoconstrictor responsiveness would be blunted and NO-mediated inhibition of sympathetic vasoconstriction would be enhanced in females compared with males. Male (M; n = 8) and female (F; n = 10) Sprague-Dawley rats were anesthetized and surgically 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 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 NOS blockade [N-omega-nitro-L-arginine methyl ester (L-NAME), 10 mg/kg iv]. At rest, sympathetic vasoconstrictor responsiveness was augmented (P < 0.05) in female compared with male rats at 2 Hz [F: -33 +/- 8% (SD); M: -26 +/- 6%] but was not different at 5 Hz (F: -55 +/- 7%; M: -47 +/- 7%). During muscle contraction, evoked vasoconstriction was similar (P < 0.05) in females and males at 2 Hz (F: -12 +/- 5%; M: -13 +/- 5%) but was blunted (P < 0.05) in females compared with males at 5 Hz (F: -24 +/- 5%; M: -34 +/- 8%). L-NAME increased (P < 0.05) sympathetic vasoconstrictor responsiveness in both groups at rest and during contraction. Contraction-mediated inhibition of vasoconstriction (sympatholysis) was enhanced (P < 0.05) in females compared with males; however, sympatholysis was not different (P < 0.05) between males and females in the presence of NOS blockade, indicating that NO-mediated sympatholysis was augmented in female rats. These data suggest that sex modulates sympathetic vascular control in resting and contracting skeletal muscle and that a portion of the enhanced sympatholysis in female rats was NO dependent.NEW & NOTEWORTHY Sex differences in the neurovascular regulation of blood pressure and vascular resistance have been documented. However, our understanding of the underlying mechanisms that mediate these differences is incomplete. The present study demonstrates that female rats have an enhanced capacity to inhibit sympathetic vasoconstriction during exercise (sympatholysis) and that NO mediates a portion of the enhanced sympatholysis.