Department of Internal Medicine, University Hospital of Pisa, Italy.
Am J Clin Nutr. 2012 Aug;96(2):302-8. doi: 10.3945/ajcn.112.035022. Epub 2012 Jun 13.
Essential hypertension is characterized by both increased oxidative stress and sympathetic traffic. Experimental studies have shown that reactive oxygen species can modulate autonomic activity.
The aim of this study was to determine whether acute administration of the antioxidant vitamin C modifies sympathetic nerve activity in essential hypertension.
Thirty-two untreated patients with essential hypertension and 20 normotensive subjects received vitamin C (3 g intravenously in 5 min) or vehicle. Heart rate, noninvasive beat-to-beat blood pressure, and muscle sympathetic nerve activity (microneurography) were monitored at baseline and up to 20 min after the infusion. Spectral analysis of RR interval variability and spontaneous baroreflex sensitivity were also computed.
Vitamin C infusion significantly lowered blood pressure in hypertensive patients but not in normotensive subjects (maximal changes in systolic blood pressure: -4.9 ± 10.1 compared with -0.7 ± 4.0 mm Hg, respectively; P < 0.05). Moreover, muscle sympathetic nerve activity was significantly reduced after vitamin C infusion in hypertensive patients (from 53.3 ± 12.2 to 47.4 ± 11.5 bursts/100 heart beats; P < 0.01) but not in healthy subjects (from 42.0 ± 10.1 to 42.7 ± 11.8 bursts/100 heart beats; NS). On the contrary, in 16 hypertensive patients, sodium nitroprusside in equidepressor doses induced a significant increase in muscle sympathetic nerve activity compared with vitamin C (+10.0 ± 6.9 bursts/100 heart beats). Sympathovagal balance and spontaneous baroreflex sensitivity were restored during vitamin C infusion in hypertensive subjects.
These results indicate that acute administration of vitamin C is able to reduce cardiovascular adrenergic drive in hypertensive patients, which suggests that oxidative stress is involved in the regulation of sympathetic activity in essential hypertension.
原发性高血压的特点是氧化应激和交感神经活动增加。实验研究表明，活性氧可以调节自主活动。
本研究旨在确定抗氧化维生素 C 的急性给药是否会改变原发性高血压患者的交感神经活性。
32 名未经治疗的原发性高血压患者和 20 名血压正常的受试者分别接受维生素 C（3 g 在 5 分钟内静脉注射）或载体。在输注前和输注后 20 分钟内监测心率、无创逐搏血压和肌肉交感神经活动（微神经记录）。还计算了 RR 间隔变异和自发性压力反射敏感性的频谱分析。
维生素 C 输注显著降低了高血压患者的血压，但对血压正常的受试者没有影响（收缩压的最大变化：-4.9 ± 10.1 与-0.7 ± 4.0 mmHg，分别；P < 0.05）。此外，维生素 C 输注后，高血压患者的肌肉交感神经活动明显降低（从 53.3 ± 12.2 到 47.4 ± 11.5 次/100 次心跳；P < 0.01），但在健康受试者中没有（从 42.0 ± 10.1 到 42.7 ± 11.8 次/100 次心跳；NS）。相反，在 16 名高血压患者中，硝普钠在等降压剂量下引起的肌肉交感神经活动增加与维生素 C 相比（+10.0 ± 6.9 次/100 次心跳）。高血压患者在维生素 C 输注期间恢复了交感神经迷走神经平衡和自发性压力反射敏感性。
这些结果表明，急性给予维生素 C 能够降低高血压患者的心血管肾上腺素能驱动，这表明氧化应激参与了原发性高血压患者交感神经活性的调节。
