Abboud F M
Clin Exp Hypertens A. 1984;6(1-2):43-60. doi: 10.3109/10641968409062550.
Sympathetic drive can contribute not only to the acute adjustment to circulatory stresses but also to sustained elevation in vascular resistance and arterial pressure. In hypertensive animals and humans excessive sympathetic activity coupled with a possible genetic factor may result in defects in electrogenic ion transport of vascular muscle or in excessive vascular hypertrophy. Increased sympathetic activity and release of the neurotransmitter may occur as a result of defects of the efferent, afferent or central components of the sympathetic system. Several studies in various animal models and in humans are described to support the notion that the mosaic concept in hypertension may be embodied in a dual theory that includes a vascular muscle defect coupled with excessive sympathetic drive both of which may be of genetic or acquired origin. Almost regardless of the cause of hypertension, interruption of sympathetic efferent activity lowers arterial pressure.
交感神经驱动不仅有助于对循环应激的急性调节，还会导致血管阻力和动脉血压的持续升高。在高血压动物和人类中，过度的交感神经活动加上可能的遗传因素，可能导致血管平滑肌电生性离子转运缺陷或血管过度肥大。交感神经系统的传出、传入或中枢成分的缺陷可能导致交感神经活动增加和神经递质释放。本文描述了在各种动物模型和人类中的多项研究，以支持以下观点：高血压的镶嵌概念可能体现在一种双重理论中，该理论包括血管平滑肌缺陷和过度的交感神经驱动，两者可能源于遗传或后天因素。几乎无论高血压的病因如何，中断交感神经传出活动都会降低动脉血压。
