Julius S
University of Michigan Medical Center, Ann Arbor.
J Hypertens Suppl. 1990 Dec;8(7):S59-65.
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.
自主神经系统的病理生理效应在高心输出量和临界高血压的年轻患者中清晰可见。随着高血压病情进展，会出现从临界高血压时的高动力循环向确诊高血压时血管阻力增加的转变。这种血流动力学转变是由β-肾上腺素能反应性降低、心脏舒张末期扩张度降低以及阻力血管α-肾上腺素能反应性增加共同引起的。同时，在高血压病程中交感神经张力会降低。交感神经张力的这种转变可以用“大脑的血压寻求特性”这一假说来解释。中枢神经系统“寻求”维持更高的血压。当血管反应过度出现时，维持神经源性高血压所需的交感神经驱动就会减少。临界高血压时的交感神经过度活跃与超重受试者、胰岛素抵抗和血脂异常有关。这提示了一个新的研究领域，即探究高血压中代谢异常的基础。
