Inhibition of ENaC by endothelin-1. Vitam Horm 2015;98:155-87
Date
03/31/2015Pubmed ID
25817869Pubmed Central ID
PMC4950931DOI
10.1016/bs.vh.2015.01.001Scopus ID
2-s2.0-84955632092 (requires institutional sign-in at Scopus site) 14 CitationsAbstract
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 AAuthor
Andrey Sorokin PhD Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBlood Pressure
Endothelin-1
Epithelial Sodium Channels
Homeostasis
Humans
Sodium
