Exercise training improves functional sympatholysis in spontaneously hypertensive rats through a nitric oxide-dependent mechanism.
Exercise training improves functional sympatholysis in spontaneously hypertensive rats through a nitric oxide-dependent mechanism.
复制标题
DOI：
10.1152/ajpheart.00103.2014
复制
发表时间：
2014-07
期刊：
影响因子：
--
通讯作者：
M. Mizuno;G. Iwamoto;W. Vongpatanasin;Jere H. Mitchell;Scott A. Smith
中科院分区：
文献类型：
--
作者：
M. Mizuno;G. Iwamoto;W. Vongpatanasin;Jere H. Mitchell;Scott A. Smith
高血压动物和患者的功能性交感神经溶解功能受损。运动训练(ET)通过一氧化氮(NO)依赖机制改善正常血压大鼠的功能性交感神经溶解。然而，ET在高血压中是否具有类似的生理益处仍有待阐明。因此，我们验证了ET通过NO依赖机制逆转高血压功能性交感神经损害的假说。在未训练的血压正常的Wistar-京都大鼠(WKYUT；n=13)、未训练的自发性高血压大鼠(SHRUT；n=13)和运动训练的自发性高血压大鼠(SHRET；n=6)上，观察了刺激腰交感神经(1、2.5和5 Hz)时股血管电导(FVC)在安静和肌肉收缩时的变化。功能性交感反应的幅度(Δ%FVC=Δ%FVC肌肉收缩-Δ%FVC静息)显著低于WKYUT(1赫兹：-2±4比13±3%；2.5赫兹：9±3比21±3%；5赫兹：12±3比26±3%；P<；0.05)。自主车轮运动3个月后，SHRET的最大摄氧量较未训练的SHRUT显著增加(78±6vs.62±4ml·kg(-1)·min(-1；P<；0.05)，并恢复了SHRET的功能性交感反应幅度(1 Hz：9±2%；2.5 Hz：20±4%；5 Hz：34±5%)。N(G)-硝基-L-精氨酸甲酯阻断一氧化氮合酶可减弱WKYUT的功能性交感反应，但不能减弱SHRUT。此外，抑制一氧化氮合酶显著降低SHRET对功能性交感神经溶解的改善。这些数据表明，在高血压大鼠中，功能性交感神经的损害是通过自主车轮运动的NO机制正常化的。
Functional sympatholysis is impaired in hypertensive animals and patients. Exercise training (ET) improves functional sympatholysis through a nitric oxide (NO)-dependent mechanism in normotensive rats. However, whether ET has similar physiological benefits in hypertension remains to be elucidated. Thus we tested the hypothesis that the impairment in functional sympatholysis in hypertension is reversed by ET through a NO-dependent mechanism. In untrained normotensive Wistar-Kyoto rats (WKYUT; n = 13), untrained spontaneously hypertensive rats (SHRUT; n = 13), and exercise-trained SHR (SHRET; n = 6), changes in femoral vascular conductance (FVC) were examined during lumbar sympathetic nerve stimulation (1, 2.5, and 5 Hz) at rest and during muscle contraction. The magnitude of functional sympatholysis (Δ%FVC = Δ%FVC muscle contraction - Δ%FVC rest) in SHRUT was significantly lower than WKYUT (1 Hz: -2 ± 4 vs. 13 ± 3%; 2.5 Hz: 9 ± 3 vs. 21 ± 3%; and 5 Hz: 12 ± 3 vs. 26 ± 3%, respectively; P < 0.05). Three months of voluntary wheel running significantly increased maximal oxygen uptake in SHRET compared with nontrained SHRUT (78 ± 6 vs. 62 ± 4 ml·kg(-1)·min(-1), respectively; P < 0.05) and restored the magnitude of functional sympatholysis in SHRET (1 Hz: 9 ± 2%; 2.5 Hz: 20 ± 4%; and 5 Hz: 34 ± 5%). Blockade of NO synthase (NOS) by N(G)-nitro-l-arginine methyl ester attenuated functional sympatholysis in WKYUT but not SHRUT. Furthermore, NOS inhibition significantly diminished the improvements in functional sympatholysis in SHRET. These data demonstrate that impairments in functional sympatholysis are normalized via a NO mechanism by voluntary wheel running in hypertensive rats.