Granger J P, Alexander B T
Department of Physiology and Biophysics and The Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi 39216-4505, USA.
Acta Physiol Scand. 2000 Jan;168(1):161-8. doi: 10.1046/j.1365-201x.2000.00655.x.
The kidneys have a critical role in long-term control of arterial pressure by regulating extracellular fluid and plasma volume. According to the renal body fluid feedback mechanism for long-term control, persistent hypertension can only occur as a result of a reduction in renal sodium excretory function or a hypertensive shift in the pressure-natriuresis relationship. Although an abnormal relationship between renal perfusion pressure and renal sodium excretion has been identified in every type of hypertension where it has been sought, factors responsible for this effect are still unclear. Nitric oxide (NO) is produced within the kidney and plays an important role in the control of many intrarenal processes which regulate the renal response to changes in perfusion pressure and thus, help determine plasma volume and blood pressure. Numerous studies have shown that long-term inhibition of NO synthesis results in a chronic rightward shift and marked attenuation in renal pressure-natriuresis. Recent studies have shown that certain animal models of genetic hypertension and forms of human hypertension areas are associated with a decrease in NO synthesis. Reductions in NO synthesis reduces renal sodium excretory function not only through direct actions on the renal vasculature, but through modulation of other vasoconstrictor processes and through direct and indirect alterations in tubular sodium transport. The causes and consequences of the dysregulation of NO in hypertension and other renal disease processes remain an important area of investigation.
肾脏在通过调节细胞外液和血浆容量来长期控制动脉血压方面发挥着关键作用。根据长期控制的肾体液反馈机制，持续性高血压仅在肾钠排泄功能降低或压力-利钠关系出现高血压性偏移时才会发生。尽管在已研究的每种高血压类型中都发现了肾灌注压与肾钠排泄之间的异常关系，但造成这种影响的因素仍不清楚。一氧化氮（NO）在肾脏内产生，在控制许多肾内过程中发挥重要作用，这些过程调节肾脏对灌注压变化的反应，从而有助于确定血浆容量和血压。大量研究表明，长期抑制NO合成会导致肾压力-利钠关系出现慢性右移并显著减弱。最近的研究表明，某些遗传性高血压动物模型和人类高血压类型与NO合成减少有关。NO合成减少不仅通过对肾血管系统的直接作用，还通过调节其他血管收缩过程以及通过对肾小管钠转运的直接和间接改变来降低肾钠排泄功能。高血压和其他肾脏疾病过程中NO失调的原因和后果仍然是一个重要的研究领域。
