Cho J H, Musch M W, Bookstein C M, McSwine R L, Rabenau K, Chang E B
Department of Medicine, University of Chicago Hospitals, Illinois 60637, USA.
Am J Physiol. 1998 Mar;274(3):C586-94. doi: 10.1152/ajpcell.1998.274.3.C586.
Na+ retention by the colon in response to salt deprivation is mediated in part by the resulting secondary hyperaldosteronism. We show that experimental hyperaldosteronism, to levels seen with salt deprivation, causes an increase in the selective expression and activity of NHE3, an apically located isoform of the Na+/H+ exchange family that functions in transepithelial Na+ absorption. The effect of aldosterone on NHE3 expression is tissue specific, occurring in intestine and not in kidney. Within the intestine, these effects are regional, being observed only in proximal colon, and different in distribution from that observed with glucocorticoids, where the predominant effect occurs in ileum. Although glucocorticoids are well known to exert many effects via regulation of transcript levels, the present study demonstrates that aldosterone stimulates intestinal Na+ absorption by increasing cellular NHE3 expression, a response that is tissue and region specific.
结肠对盐缺乏的钠潴留反应部分是由继发性醛固酮增多症介导的。我们发现，实验性醛固酮增多症达到盐缺乏时的水平，会导致NHE3（一种位于顶端的Na+/H+交换家族异构体，在跨上皮钠吸收中起作用）的选择性表达和活性增加。醛固酮对NHE3表达的影响具有组织特异性，发生在肠道而非肾脏。在肠道内，这些影响具有区域性，仅在近端结肠观察到，且分布与糖皮质激素不同，糖皮质激素的主要作用发生在回肠。尽管众所周知糖皮质激素通过调节转录水平发挥多种作用，但本研究表明醛固酮通过增加细胞NHE3表达来刺激肠道钠吸收，这种反应具有组织和区域特异性。
