Changing role of the autonomic nervous system in human hypertension.
Changing role of the autonomic nervous system in human hypertension.
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发表时间：
1990-12
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通讯作者：
S. Julius
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作者：
S. Julius
在具有高心输出量和临界高血压的年轻患者中可以清楚地看到自主神经系统的病理生理学影响。随着高血压的进展，从临界高血压中的过度运动循环转变为已建立的高血压中所见的血管阻力增加。这种血流动力学转变是由β-肾上腺素能反应性降低和心脏舒张末期扩张减少以及阻力血管的α-肾上腺素能反应性增加引起的。与此同时，高血压病程中交感神经张力减弱。交感神经张力的这种转变可以通过“大脑的血压寻求特性”的假设来解释。中枢神经系统“寻求”维持较高的压力。当血管过度反应出现时，需要较少的交感神经驱动来维持神经源性高血压。临界高血压的交感神经过度活跃与超重、胰岛素抵抗和血脂异常有关。这提出了一个新的研究领域来调查高血压代谢异常的基础。
Pathophysiological effects of the autonomic nervous system are clearly seen in young patients with a high cardiac output and borderline hypertension. As the hypertension progresses, there is a change from the hyperkinetic circulation in borderline hypertension to the increased vascular resistance seen in established hypertension. This hemodynamic transition is caused by decreased beta-adrenergic responsiveness and decreased end-diastolic distension of the heart combined with an increased alpha-adrenergic responsiveness of the resistance vessels. In parallel, the sympathetic tone decreases in the course of hypertension. This transition in sympathetic tone can be explained by the hypothesis of the 'blood pressure seeking properties of the brain'. The central nervous system 'seeks' to maintain a higher pressure. When vascular overresponsiveness sets in, less sympathetic drive is needed to maintain a neurogenic hypertension. Sympathetic overactivity in borderline hypertension is associated with overweight subjects, insulin resistance and dyslipidemia. This suggests a new area of research to investigate the basis of metabolic abnormalities in hypertension.