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交感神经在原发性高血压发病机制中的作用

Sympathetic nerves effect in essential hypertention pathogenesis

  • 摘要: 原发性高血压发病机制复杂,既有遗传因素也有环境刺激因素。不断累积的证据显示大多数原发性高血压是调控功能紊乱的结果,主要缘于升压效应过强,强过了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。业内普遍认可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随功能加强、交感神经之间固有的相互抑制能力降低等方面。

     

    Abstract: The pathogenesis of essential hypertension is complicated, involving both genetic susceptibility and environmental stimuli. Accumulating evidence demonstrate most essential hypertention result from dysfunction of pressure regulation, due to strong elevated effects mainly, stronger than body abilities to balance blood pressure. Sympathetic nerves tension, renin-angiotensin-aldosterone system and renal water-sodium retention is the major role in raising blood pressure, and sympathetic nerves activity is the ligament among three. Abnormal activated sympathetic nerves or increased aldosterone secretion are initial factors of causing hypertention has been well received. Abnormal activation of sympathetic nerves may be partly due to coupling sympathetic nerves structure change with function strengthen, or decreased innate inhibition ability among sympathetic nerves each other.

     

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