Vercellotti G M, Tolins J P
Department of Medicine, University of Minnesota, Minneapolis 55455.
Am J Kidney Dis. 1993 Mar;21(3):331-43. doi: 10.1016/s0272-6386(12)80757-8.
We have come to appreciate that the endothelium plays a major role in regulation of renal hemodynamics and excretory function. In the normal state, the endothelium maintains an intricate balance of interacting relaxing and contracting factors that can influence vasomotor tone and renal sodium handling, but also plays a role in the control of the coagulation system and cellular proliferation. Studies of reactive oxygen species as mediators of endothelial injury have shown that the perturbed endothelium can respond to such a threat, calling on intrinsic protective mechanisms such as induction of heme oxygenase and ferritin synthesis. In vivo studies have demonstrated that these mechanisms may confer protection in experimental models of acute renal injury. However, when endothelial injury or dysfunction does occur, adverse renal hemodynamic consequences, systemic hypertension, enhanced platelet aggregation, and mesangial cell proliferation could all contribute to progressive renal dysfunction. The role of the endothelium in modulation of normal renal function and in the pathogenesis of renal diseases will be the focus of future research efforts.
我们已经认识到内皮细胞在调节肾血流动力学和排泄功能中起主要作用。在正常状态下，内皮细胞维持着相互作用的舒张和收缩因子的复杂平衡，这些因子可影响血管舒缩张力和肾钠处理，而且在凝血系统控制和细胞增殖中也发挥作用。作为内皮损伤介质的活性氧研究表明，受扰动的内皮细胞能够对这种威胁做出反应，启动诸如诱导血红素加氧酶和铁蛋白合成等内在保护机制。体内研究已证明，这些机制可能在急性肾损伤实验模型中提供保护。然而，当内皮损伤或功能障碍确实发生时，不良的肾血流动力学后果、全身性高血压、血小板聚集增强和系膜细胞增殖都可能导致进行性肾功能障碍。内皮细胞在调节正常肾功能和肾脏疾病发病机制中的作用将是未来研究工作的重点。
