Winquist R J, Webb R C, Bohr D F
Fed Proc. 1982 Jun;41(8):2387-93.
The cause of the elevated arterial pressure in most forms of hypertension is an increase in total peripheral resistance. This brief review is directed toward an assessment of recent investigations contributing information about the factors responsible for this increased vascular resistance. Structural abnormalities in the vasculature that characterize the hypertensive process are 1) changes in the vascular media, 2) rarefication of the resistance vessels, and 3) lesions of the intimal vascular surface. These abnormalities are mainly the result of an adaptive process and are secondary to the increase in wall stress and/or to pathological damage to cellular components in the vessel wall. Functional alterations in the vascular smooth muscle are described as changes in agonist-smooth muscle interaction or plasma membrane permeability. These types of changes appear to play a primary, initiating role in the elevation of vascular resistance of hypertension. These alterations are not the result of an increase in wall stress and they often precede the development of high blood pressure. The functional changes are initiated by abnormal function of neurogenic, humoral, and/or myogenic changes that alter vascular smooth muscle activity.
大多数高血压类型中动脉压升高的原因是总外周阻力增加。本简要综述旨在评估近期的研究，这些研究提供了有关导致这种血管阻力增加的因素的信息。高血压过程中血管系统的结构异常包括：1）血管中膜的变化；2）阻力血管稀疏；3）内膜血管表面病变。这些异常主要是适应性过程的结果，继发于壁应力增加和/或血管壁细胞成分的病理损伤。血管平滑肌的功能改变表现为激动剂与平滑肌相互作用或质膜通透性的变化。这些类型的变化似乎在高血压血管阻力升高过程中起主要的起始作用。这些改变不是壁应力增加的结果，并且它们通常在高血压发展之前出现。功能改变是由改变血管平滑肌活动的神经源性、体液性和/或肌源性变化的异常功能引发的。
