Endothelin and Renal Ion and Water Transport

Academic Article

Abstract

  • © 2015 Elsevier Inc. 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.
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    Published In

    Digital Object Identifier (doi)

    Author List

  • Speed JS; Fox BM; Johnston JG; Pollock DM
  • Start Page

  • 137
  • End Page

  • 144
  • Volume

  • 35
  • Issue

  • 2