Weber C S, Thayer J F, Rudat M, Sharma A M, Perschel F H, Buchholz K, Deter H C
Department of Psychosomatic Medicine and Psychotherapy, Charité Universitätsmedizin, Berlin, Germany.
J Hum Hypertens. 2008 Jun;22(6):423-31. doi: 10.1038/jhh.2008.11. Epub 2008 Mar 13.
Salt sensitivity (SS) represents a risk factor for essential hypertension, which has been related to enhanced cardiovascular stress reactivity possibly mediated by increased noradrenergic susceptibility. We investigated biophysiological responses to mental stress in salt-sensitive (ss) and salt-resistant (sr) subjects, hypothesizing lower heart rate variability (HRV) and higher cortisol in the ss. A total of 48 healthy normotensive Caucasian men (age 25.6+/-2.6, body mass index 22.9+/-2.3) were phenotyped for SS (defined as significant drop in mean arterial pressure>3 mm Hg under the low-salt diet) by a 2-week high- versus low-salt diet. Subjects underwent a standardized mental stress task with continuous cardiovascular monitoring before, during and after the test (Finapres; Ohmeda, Louisville, CO, USA). Blood samples were drawn to examine cortisol and catecholamines before, after and 20 min after stress. The task elicited significant increases of systolic blood pressure (SBP), diastolic BP (DBP) and heart rate (HR) and a significant decrease of HRV (all time effects P<0.0001). The ss subjects showed lower norepinephrine (NE) and higher cortisol, indicated by significant group effects (P=0.009 and 0.025, respectively). HR increased and HRV decreased more in the ss under the stress, shown by significant time by group interactions (P=0.045 and 0.003, respectively). The observation of a more pronounced HR rise coupled with a greater decrease of HRV in healthy ss men under the influence of brief mental stress confirms their enhanced physiological stress reactivity. The lower peripheral NE may represent an effort to compensate for increased noradrenergic receptor sensitivity. The enhanced cortisol levels are backed by recent genetic findings on HSD11B2 polymorphisms and may promote hypertension.
盐敏感性（SS）是原发性高血压的一个危险因素，它可能与去甲肾上腺素能易感性增加介导的心血管应激反应增强有关。我们研究了盐敏感（ss）和盐抵抗（sr）受试者对精神应激的生物生理反应，假设盐敏感者心率变异性（HRV）较低且皮质醇水平较高。通过为期2周的高盐饮食与低盐饮食，对总共48名健康的血压正常的白种男性（年龄25.6±2.6，体重指数22.9±2.3）进行盐敏感性表型分析（定义为低盐饮食下平均动脉压显著下降>3 mmHg）。受试者在测试前、测试期间和测试后接受标准化精神应激任务，并进行连续心血管监测（Finapres；美国俄亥俄州路易斯维尔市的Ohmeda公司）。在应激前、应激后和应激后20分钟采集血样检测皮质醇和儿茶酚胺。该任务引起收缩压（SBP）、舒张压（DBP）和心率（HR）显著升高，HRV显著降低（所有时间效应P<0.0001）。盐敏感受试者的去甲肾上腺素（NE）水平较低，皮质醇水平较高，具有显著的组间效应（分别为P = 0.009和0.025）。在应激状态下，盐敏感者HR升高且HRV下降更为明显，具有显著的时间×组间交互作用（分别为P = 0.045和0.003）。观察到在短暂精神应激影响下，健康盐敏感男性HR上升更为明显且HRV下降幅度更大，证实了他们增强的生理应激反应性。外周NE水平较低可能是为了补偿去甲肾上腺素能受体敏感性增加。皮质醇水平升高得到了近期关于HSD11B2多态性的遗传学研究结果的支持，可能会促进高血压的发生。
