CLINICAL PHYSIOLOGY OF HYPERTENSION

我们发现年轻的原发性高血压患者 肱动脉重搏波的调制缺陷。 的循环 我们开发的模型解释了增加的异常 动脉硬化和血管舒张反应性降低。 幅度 的缺陷与交感神经活动有关， 去甲肾上腺素（NE）、交感神经系统 神经传递素 利用动脉脉搏波速度和前臂 体积描记术以指示肱动脉僵硬度和平均小动脉 口径，我们计划确定动脉的单独贡献 僵硬和血管扩张失败的血管异常， 在原发性高血压的发展早期。 试点结果表明， 动脉硬化--真正的动脉硬化--可能 根据测量结果导致动脉内压高估， 袖口，这种僵硬可能有神经性成分。

We have found that young patients with essential hypertension have defective modulation of the brachial arterial dicrotic wave. A circulatory model which we developed explains the abnormality in terms of increased arterial rigidity and decreased vasodilator responsiveness. The magnitude of the defect was related to sympathetic neural activity as reflected by arterial plasma concentrations of norepinephrine (NE), the sympathetic neurotransmitter. Using arterial pulse wave velocity and forearm plethysmography to indicate brachial arterial stiffness and mean arteriolar caliber, we plan to determine the separate contributions of arterial rigidity and vasodilatory failure to the vascular abnormalities which occur early in the development of essential hypertension. Pilot results suggest the possibility that arterial stiffness -- true arteriosclerosis -- may cause overestimation of intra-arterial pressure based on measurements by cuff, and this stiffness may have a neurogenic component.