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1: Am J Physiol Renal Physiol. 2008 Oct;295(4):F1063-70. Epub 2008 Jul 30.
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Regulation of the epithelial Na+ channel by endothelin-1 in rat collecting duct.

Bugaj V, Pochynyuk O, Mironova E, Vandewalle A, Medina JL, Stockand JD.

Department of Physiology 7756, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.

We used patch-clamp electrophysiology to investigate regulation of the epithelial Na+ channel (ENaC) by endothelin-1 (ET-1) in isolated, split-open rat collecting ducts. ET-1 significantly decreases ENaC open probability by about threefold within 5 min. ET-1 decreases ENaC activity through basolateral membrane ETB but not ETA receptors. In rat collecting duct, we find no role for phospholipase C or protein kinase C in the rapid response of ENaC to ET-1. ET-1, although, does activate src family tyrosine kinases and their downstream MAPK1/2 effector cascade in renal principal cells. Both src kinases and MAPK1/2 signaling are necessary for ET-1-dependent decreases in ENaC open probability in the split-open collecting duct. We conclude that ET-1 in a physiologically relevant manner rapidly suppresses ENaC activity in native, mammalian principal cells. These findings may provide a potential mechanism for the natriuresis observed in vivo in response to ET-1, as well as a potential cause for the salt-sensitive hypertension found in animals with impaired endothelin signaling.

Publication Types:
PMID: 18667482 [PubMed - indexed for MEDLINE]

PMCID: PMC2576140 [Available on 2009/10/01]