Norlander Allison E, Madhur Meena S
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville Tennesee; and.
Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville Tennesee; and
Am J Physiol Renal Physiol. 2017 Aug 1;313(2):F141-F144. doi: 10.1152/ajprenal.00465.2016. Epub 2017 Apr 12.
Hypertension is growing in epidemic proportions worldwide and is now the leading preventable cause of premature death. For over a century, we have known that the kidney plays a critical role in blood pressure regulation. Specifically, abnormalities in renal sodium transport appear to be a final common pathway that gives rise to elevated blood pressure regardless of the nature of the initial hypertensive stimulus. However, it is only in the past decade that we have come to realize that inflammatory cytokines secreted by innate and adaptive immune cells, as well as renal epithelial cells, can modulate the expression and activity of sodium transporters all along the nephron, leading to alterations in pressure natriuresis, sodium and water balance, and ultimately hypertension. This mini-review highlights specific cytokines and the transporters that they regulate and discusses why inflammatory cytokines may have evolved to serve this function.
高血压在全球正呈流行趋势增长,目前是可预防的过早死亡的主要原因。一个多世纪以来,我们已经知道肾脏在血压调节中起着关键作用。具体而言,肾钠转运异常似乎是导致血压升高的最终共同途径,而无论初始高血压刺激的性质如何。然而,直到过去十年我们才开始意识到,先天免疫细胞、适应性免疫细胞以及肾上皮细胞分泌的炎性细胞因子可调节整个肾单位钠转运体的表达和活性,从而导致压力性利钠、钠和水平衡改变,最终引发高血压。这篇小型综述重点介绍了特定的细胞因子及其调节的转运体,并讨论了炎性细胞因子为何可能进化出这种功能。