Speed Joshua S, Fox Brandon M, Johnston Jermaine G, Pollock David M
Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
Semin Nephrol. 2015 Mar;35(2):137-44. doi: 10.1016/j.semnephrol.2015.02.003.
The renal tubular epithelial cells produce more endothelin-1 (ET-1) than any other cell type in the body. Moving down the nephron, the amount of ET-1 produced appears fairly consistent until reaching the inner medullary collecting duct, which produces at least 10 times more ET-1 than any other segment. ET-1 inhibits Na(+) transport in all parts of the nephron through activation of the ETB receptor, and, to a minor extent, the ETA receptor. These effects are most prominent in the collecting duct where ETB-receptor activation inhibits activity of the epithelial Na(+) channel. Effects in other parts of the nephron include inhibition of Na(+)/H(+) exchange in the proximal tubule and the Na(+), K(+), 2Cl(-) co-transporter in the thick ascending limb. In general, the renal epithelial ET-1 system is an integral part of the body's response to a high salt intake to maintain homeostasis and normal blood pressure. Loss of ETB-receptor function results in salt-sensitive hypertension. The role of renal ET-1 and how it affects Na(+) and water transport throughout the nephron is reviewed.
肾小管上皮细胞产生的内皮素-1（ET-1）比体内任何其他细胞类型都多。沿着肾单位向下，ET-1的产生量在到达内髓集合管之前似乎相当稳定，而内髓集合管产生的ET-1比其他任何节段至少多10倍。ET-1通过激活ETB受体，在较小程度上也通过激活ETA受体，抑制肾单位各部位的Na(+)转运。这些作用在集合管最为显著，ETB受体激活可抑制上皮Na(+)通道的活性。在肾单位其他部位的作用包括抑制近端小管中的Na(+)/H(+)交换以及厚壁升支中的Na(+)、K(+)、2Cl(-)共转运体。一般来说，肾上皮ET-1系统是机体对高盐摄入作出反应以维持体内平衡和正常血压的一个组成部分。ETB受体功能丧失会导致盐敏感性高血压。本文综述了肾ET-1的作用及其如何影响整个肾单位的Na(+)和水转运。
