Endothelin and Renal Ion and Water Transport #MMPMID25966345
Speed JS; Fox BM; Johnston JG; Pollock DM
Semin Nephrol 2015[Mar]; 35 (2): 137-44 PMID25966345show ga
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 in order to maintain homeostasis and normal blood pressure. Loss of ETB receptor function results in salt sensitive hypertension. The goal of this article is to review the role of renal ET-1 and how it affects Na+ and water transport throughout the nephron.