交感神经在原发性高血压发病机制中的作用

原发性高血压发病机制复杂,既有遗传因素也有环境因素。大量研究表明,大多数原发性高血压是调控功能紊乱的结果,主要为升压效应过强,并大于机体平衡血压的能力。交感神经的紧张性活动、肾素-血管紧张素-醛固酮系统激活、肾水钠潴留是主要的升压途径。交感神经的活动是三者联系的纽带。目前普遍认为交感神经的异常激活和醛固酮释放增多是原发性高血压主要的始动因素。交感神经的异常激活可能部分归因于交感神经结构改变伴功能加强、交感神经之间固有的相互抑制能力降低等。

Sympathetic nerves effect in essential hypertention pathogenesis

The pathogenesis of essential hypertension is complicated, involving both genetic susceptibility and environmental stimuli. A large number of studies demonstrate that most essential hypertension results from dysfunction of pressure regulation, mainly due to too strong elevated effects, which are stronger than the body''s ability to balance blood pressure. The tension of sympathetic nerves, activation of the renin-angiotensin-aldosterone system, and renal water-sodium retention are the main ways of increasing the pressure, and sympathetic nerve activity is the link between the three. It is generally believed that abnormal sympathetic nerve activation and increased release of aldosterone are major initiating factors of essential hypertension. The abnormal activation of sympathetic nerves may be partly due to structural changes of sympathetic nerves coupled with functional enhancement, and the decreased innate ability of mutual inhibition between sympathetic nerves.