Clinica Medica, Ospedale S. Gerardo dei Tintori, Via Pergolesi 33, 20052 Monza, Milan, Italy.
Exp Physiol. 2010 May;95(5):581-6. doi: 10.1113/expphysiol.2009.047381. Epub 2009 Dec 11.
Data collected in experimental animals and in humans support the hypothesis that sympathetic neural mechanisms are involved in the development and progression of hypertension. Direct approaches to assess human adrenergic cardiovascular drive have shown that sympathetic activation occurs in hypertensive patients, the magnitude of which is proportional to the degree of elevation of the blood pressure. Evidence has also been obtained that sympathetic activation participates in the development of hypertension-related target organ damage, such as left ventricular diastolic dysfunction, left ventricular hypertrophy and arterial remodelling and hypertrophy. Despite the large amount of information collected on the main features of the hypertension-related neurogenic abnormality, the causes of the sympathetic activation remain undefined, although alterations in the reflex modulation of adrenergic drive and/or participation of metabolic factors are likely candidates. This paper will provide background information on the behaviour of the sympathetic nervous system in experimental hypertension, followed by a review of the main features, mechanisms and effects of the sympathetic overdrive in human hypertension. Finally, the new frontiers of research in the area of therapeutic intervention aimed at reducing the adrenergic overdrive will be highlighted.
在实验动物和人类中收集的数据支持这样一种假设，即交感神经机制参与了高血压的发生和发展。评估人类肾上腺素能心血管驱动力的直接方法表明，高血压患者存在交感神经激活，其程度与血压升高的幅度成正比。还有证据表明，交感神经激活参与了与高血压相关的靶器官损伤的发生，如左心室舒张功能障碍、左心室肥厚以及动脉重塑和肥厚。尽管已经收集了大量关于与高血压相关的神经源性异常的主要特征的信息，但交感神经激活的原因仍未确定，尽管肾上腺素能驱动的反射调节改变和/或代谢因素的参与可能是候选因素。本文将提供实验性高血压中交感神经系统行为的背景信息，然后回顾人类高血压中交感神经过度驱动的主要特征、机制和影响。最后，将强调旨在减少肾上腺素能过度驱动的治疗干预领域的新研究前沿。
