Granger J P, Schnackenberg C G
Department of Physiology and Biophysics and The Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson 39216-4505, USA.
Semin Nephrol. 2000 Sep;20(5):417-25.
The kidneys play a central role in the long-term control of arterial pressure by regulating sodium balance and extracellular fluid volume. The renin-angiotensin system is important in the regulation of the arterial pressure through its chronic effects on the pressure natriuresis relationship. Under physiologic conditions, angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain sodium balance in response to variations in sodium intake. An inability to suppress Ang II formation in response to increases in sodium intake can lead to salt-sensitive hypertension. Excess formation of Ang II, such as in renovascular hypertension, causes the pressure natriuresis relationship to be shifted to higher arterial pressures so that higher arterial pressures are necessary to maintain sodium balance. Ang II decreases pressure natriuresis by enhancing tubular reabsorption and/or reducing glomerular filtration. Because Ang II does not decrease glomerular filtration in most circumstances, the sodium retaining actions of Ang II are usually caused by increased tubular reabsorption. However, there are a number of pathophysiologic conditions where Ang II interacts with various local autocrine and paracrine factors (such as nitric oxide [NO], eicosanoids, adenosine, and superoxide) to influence glomerular filtration rate. Ang II enhances tubular reabsorption either indirectly, through aldosterone stimulation, via alterations in renal hemodynamics (physical factors or medullary blood flow), or by directly enhancing tubular sodium transport. Converting enzyme inhibitors or Ang II receptor antagonists improve pressure natriuresis and are very effective in the treatment of various forms of hypertension associated with normal or enhanced activity of the renin-angiotensin system.
肾脏通过调节钠平衡和细胞外液量在动脉血压的长期控制中发挥核心作用。肾素-血管紧张素系统通过其对压力-利钠关系的慢性影响在动脉血压调节中起重要作用。在生理条件下，血管紧张素II（Ang II）对于使动脉血压与钠排泄之间的长期关系变得非常陡峭很重要，这样在应对钠摄入变化时，只需动脉血压发生极小的变化就能维持钠平衡。因钠摄入增加而无法抑制Ang II的生成会导致盐敏感性高血压。Ang II生成过多，如在肾血管性高血压中，会使压力-利钠关系向更高的动脉血压偏移，从而需要更高的动脉血压来维持钠平衡。Ang II通过增强肾小管重吸收和/或降低肾小球滤过率来降低压力-利钠作用。由于在大多数情况下Ang II不会降低肾小球滤过率，所以Ang II的保钠作用通常是由肾小管重吸收增加引起的。然而，在一些病理生理情况下，Ang II会与各种局部自分泌和旁分泌因子（如一氧化氮[NO]、类二十烷酸、腺苷和超氧化物）相互作用，以影响肾小球滤过率。Ang II通过刺激醛固酮、改变肾血流动力学（物理因素或髓质血流量）间接增强肾小管重吸收，或直接增强肾小管钠转运。转换酶抑制剂或Ang II受体拮抗剂可改善压力-利钠作用，对治疗与肾素-血管紧张素系统活性正常或增强相关的各种形式的高血压非常有效。
