Buchholz Konrad, Schächinger Hartmut, Wagner Miriam, Sharma Arya M, Deter Hans Christian
Division of Psychosomatic Medicine, Benjamin Franklin Medical Center, Free University of Berlin, Berlin, Germany.
Am J Hypertens. 2003 Jul;16(7):531-6. doi: 10.1016/s0895-7061(03)00905-1.
Salt-sensitive normotensive men exhibit an enhanced pressor and heart rate (HR) response to mental stress. Stress-induced HR acceleration may result from sympathetic activation or vagal withdrawal. We studied the importance of vagal withdrawal for the increased stress responsiveness of salt-sensitive subjects.
We studied cardiovascular reactivity to mental challenge in 17 salt-sensitive healthy white male students and 56 salt-resistant control subjects who were comparable with respect to age, body mass index, and physical fitness. Salt sensitivity was determined by a 2-week dietary protocol (20 mmol v 240 mmol sodium/day). Mental stress was induced by a computerized information-processing task (manometer test). Electrocardiogram and finger blood pressure (BP; Finapres, Ohmeda, Louisville, CO) were registered continuously to determine HR and interbeat-interval length. Time and frequency domain (spectral power) based measures of respiratory-related heart rate variability (HRV) were calculated to estimate vagal cardiac control; diastolic BP reactivity was assessed to estimate peripheral sympathetic effects.
Stress-induced increase in HR was higher in salt-sensitive than in salt-resistant subjects. Salt-sensitive subjects, in comparison to salt-resistant subjects, showed significantly reduced respiratory-related HRV during baseline and mental stress conditions (P <.01). The increase in diastolic BP during mental challenge was significantly greater in salt-sensitive subjects (P <.05).
Our findings suggest reduced vagal and increased sympathetic tone during mental challenge in salt-sensitive subjects. Altered autonomic nervous system function may contribute to later development of hypertension in salt-sensitive individuals.
盐敏感的血压正常男性对精神应激表现出增强的升压和心率（HR）反应。应激诱导的心率加速可能源于交感神经激活或迷走神经撤离。我们研究了迷走神经撤离对盐敏感受试者应激反应性增加的重要性。
我们研究了17名盐敏感的健康白人男性学生和56名盐抵抗对照受试者对精神挑战的心血管反应性，这些受试者在年龄、体重指数和身体素质方面具有可比性。盐敏感性通过为期2周的饮食方案（20 mmol对240 mmol钠/天）来确定。通过计算机化信息处理任务（压力计测试）诱导精神应激。连续记录心电图和手指血压（BP；Finapres，Ohmeda，路易斯维尔，科罗拉多州）以确定心率和心跳间期长度。计算基于时间和频域（频谱功率）的呼吸相关心率变异性（HRV）测量值以估计迷走神经对心脏的控制；评估舒张压反应性以估计外周交感神经效应。
应激诱导的心率增加在盐敏感受试者中高于盐抵抗受试者。与盐抵抗受试者相比，盐敏感受试者在基线和精神应激条件下呼吸相关HRV显著降低（P<.01）。精神挑战期间盐敏感受试者的舒张压升高显著更大（P<.05）。
我们的研究结果表明，盐敏感受试者在精神挑战期间迷走神经张力降低，交感神经张力增加。自主神经系统功能改变可能有助于盐敏感个体后期高血压的发展。
