Ruilope L M, Lahera V, Rodicio J L, Carlos Romero J
Hospital 12 de Octubre, Departmento de Fisiologia, Facultad de Medicina, Universidad Complutense, Madrid, Spain.
Hypertension. 1994 Jan;23(1):3-9. doi: 10.1161/01.hyp.23.1.3.
The kidney plays a key role in the control of body fluids and blood pressure. Evidence has shown that impairment of renal function can lead to the development of arterial hypertension. The regulation of renal blood flow appears to be a key element in the pathophysiology of the hypertensive process, because multiple evidence suggests the existence of a functional enhancement of renal vascular tone in this disorder. The existence of renal vasoconstriction and of an inherited defect in the regulation of renal blood flow has been proposed in the prehypertensive stage. The mechanisms responsible for this alteration include a lack of modulation of the renal vasculature to angiotensin II, increased sympathetic activity, or suppressed renal dopaminergic activity. Established hypertension is characterized by elevated renal vascular resistance, decreased renal blood flow, sustained glomerular filtration rate, and increased filtration fraction. The increase in renal vascular resistance is initially due to elevations in renal vascular tone and is reversible, whereas later it becomes irreversible because of structural changes involved in nephrosclerosis. Antihypertensive drugs are able to decrease blood pressure and to prevent the development of further renal vascular damage independently of variable effects on renal hemodynamics.
肾脏在体液和血压控制中起关键作用。有证据表明,肾功能损害可导致动脉高血压的发生。肾血流的调节似乎是高血压发病机制中的一个关键因素,因为多项证据表明,在这种疾病中存在肾血管张力的功能性增强。在高血压前期阶段,有人提出存在肾血管收缩以及肾血流调节的遗传性缺陷。导致这种改变的机制包括肾血管系统对血管紧张素 II 的调节不足、交感神经活动增加或肾多巴胺能活动受抑制。确诊的高血压的特征是肾血管阻力升高、肾血流量减少、肾小球滤过率持续存在以及滤过分数增加。肾血管阻力的增加最初是由于肾血管张力升高,并且是可逆的,而后来由于肾硬化所涉及的结构变化,它变得不可逆。抗高血压药物能够降低血压,并独立于对肾血流动力学的可变影响来预防进一步的肾血管损伤。