Recent advances in the pathogenesis of hypertension: consideration of structural, functional, and metabolic vascular abnormalities resulting in elevated arterial resistance.
Recent advances in the pathogenesis of hypertension: consideration of structural, functional, and metabolic vascular abnormalities resulting in elevated arterial resistance.
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DOI：
10.1016/s0002-8703(81)80016-6
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发表时间：
1981-08
影响因子：
4.8
通讯作者：
R. Webb;D. Bohr
中科院分区：
文献类型：
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作者：
R. Webb;D. Bohr
慢性高血压（HT）的动脉压升高是由总外周血管阻力（TPVR）增加引起的。因此，从血流动力学上讲，HT是血管变化的结果。本报告的主要目的是描述目前的状态和最近的进展，特点是这种血管的变化负责HT的发展。作为理解变化本质的背景知识，探究变化的原因是有益的。通常调节血管阻力的一个或多个控制系统一定发生了什么变化。这些系统包括（1）自主神经系统，表达神经源性传入和中枢神经系统的活动;（2）肾脏，具有两个相关功能：（a）盐和水的代谢，和（B）产生具有升压或降压作用的调节激素;和（3）肾上腺皮质。这些神经源性和体液因素，沿着适当的遗传基质和环境影响，如钠摄入，以增加TPVR的方式影响阻力血管。通常很难确定启动整个过程的”原动力”。这是真实的最常见的类型的疾病，临床上必要的HT和实验自发HT的大鼠。然而，即使已知起始因素，如肾缺血或盐皮质激素过量，
The elevated arterial pressure of chronic hypertension (HT) is caused by increased total peripheral vascular resistance (TPVR). Hemodynamically, therefore, HT is the result of vascular change. The primary goal of the present presentation is to delineate the current status and recent advances that characterize this vascular change responsible for the HT development. As background knowledge for understanding the nature of the change, it is informative to inquire into the cause of the change. Something must happen to one or more of the controlling systems that normally regulate vascular resistance. These systems include (1) the autonomic nervous system which expresses activity of neurogenic afferents and of the central nervous system;(2) the kidney with two relevant functions (a) salt and water metabolism, and (b) production of regulatory hormones with either pressor or depressor actions; and (3) the adrenal cortex. These neurogenic and humoral factors, along with appropriate genetic matrix and environmental influences, such as sodium intake, affect the resistance vessels in such a way that TPVR is increased. It is usually difficult to identify the" prime mover" that initiates the overall process. This is true of the most common types of the disease, clinical essential HT and experimental spontaneous HT in the rat. However, even when the initiating factor is known, such as renal ischemia or mineralocorticoid excess, the sequence of events leading from this