title: Endothelin and renal ion and water transport.
abstract: 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.
authors.affiliation: Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
authors.forename: Joshua S
authors.initials: JS
authors.lastname: Speed
authors.affiliation: Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
authors.forename: Brandon M
authors.initials: BM
authors.lastname: Fox
authors.affiliation: Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
authors.forename: Jermaine G
authors.initials: JG
authors.lastname: Johnston
authors.affiliation: Cardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL. Electronic address: dpollock@uab.edu.
authors.forename: David M
authors.initials: DM
authors.lastname: Pollock
mesh_terms: D020346:Aquaporins / Q000378:metabolism; D016232:Endothelins / Q000378:metabolism*; D006706:Homeostasis; D006801:Humans; D017136:Ion Transport; D007685:Kidney Tubules, Collecting / Q000378:metabolism*; D007687:Kidney Tubules, Proximal / Q000378:metabolism*; D015398:Signal Transduction; D012965:Sodium Chloride / Q000378:metabolism*
chemical_list: D020346:Aquaporins; D016232:Endothelins; D012965:Sodium Chloride
keywords: Endothelin; kidney; sodium transport