Schmieder R E, Langewitz W, Otten H, Rüddel H, Schulte W, von Eiff A W
Department of Medicine, Bonn-Venusberg, FRG.
J Hum Hypertens. 1987 Dec;1(3):215-22.
Epidemiologic and experimental studies disclosed that the sympathetic nervous system might play a pivotal role in the pathogenesis of essential hypertension. Although systolic pressure exhibits a weak endogenous rhythm, diurnal fluctuations of arterial pressure are provoked primarily by physical or emotional stress factors. The magnitude of the cardiovascular response, however, varies widely from individual to individual. Subjects at high risk of future hypertension,--such as those with a positive history of familial hypertension, high resting heart rate, or transient increase in arterial hypertension--revealed blood pressure hyperresponsiveness to stress stimuli mediated by an overreactivity of the sympathetic nervous system. Furthermore, cardiovascular reactivity to mental arithmetic tasks and to traffic noise put a patient at high risk of developing arterial hypertension. In women, exaggerated cardiovascular response to stress stimuli appeared to be mitigated by estrogens, whereas oral contraceptives overrode this 'protective' effect of estrogens. At a certain point, repeated episodes of high stress blood pressure could produce structural vascular changes finally inducing sustained hypertension.
流行病学和实验研究表明，交感神经系统可能在原发性高血压的发病机制中起关键作用。虽然收缩压呈现出较弱的内源性节律，但动脉血压的昼夜波动主要由身体或情绪应激因素引起。然而，心血管反应的程度在个体之间差异很大。未来患高血压风险较高的受试者，如那些有家族性高血压阳性病史、静息心率高或动脉高血压短暂升高的人，表现出对由交感神经系统过度反应介导的应激刺激的血压高反应性。此外，对心算任务和交通噪音的心血管反应性使患者处于患动脉高血压的高风险中。在女性中，雌激素似乎减轻了对应激刺激的过度心血管反应，而口服避孕药则消除了雌激素的这种“保护”作用。在某一时刻，反复出现的高应激血压可能会导致血管结构改变，最终引发持续性高血压。
