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Inhibition of ENaC by endothelin-1. Vitam Horm 2015;98:155-87

Date

03/31/2015

Pubmed ID

25817869

Pubmed Central ID

PMC4950931

DOI

10.1016/bs.vh.2015.01.001

Scopus ID

2-s2.0-84955632092 (requires institutional sign-in at Scopus site)   14 Citations

Abstract

The amiloride-sensitive epithelial Na(+) channel (ENaC) is a key player in the regulation of Na(+) homeostasis. Its functional activity is under continuous control by a variety of signaling molecules, including bioactive peptides of endothelin family. Since ENaC dysfunction is causative for disturbances in total body Na(+) levels associated with the abnormal regulation of blood volume, blood pressure, and lung fluid balance, uncovering the molecular mechanisms of inhibitory modulation or inappropriate activation of ENaC is crucial for the successful treatment of a variety of human diseases including hypertension. The precise regulation of ENaC is particularly important for normal Na(+) and fluid homeostasis in organs where endothelins are known to act: the kidneys, lung, and colon. Inhibition of ENaC by endothelin-1 (ET-1) has been established in renal cells, and several molecular mechanisms of inhibition of ENaC by ET-1 are proposed and will be reviewed in this chapter.

Author List

Sorokin A, Staruschenko A

Author

Andrey Sorokin PhD Professor in the Medicine department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Blood Pressure
Endothelin-1
Epithelial Sodium Channels
Homeostasis
Humans
Sodium