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Regulation of the epithelial Na+ channel by endothelin-1 in rat collecting duct.
- Source :
-
American Journal of Physiology: Renal Physiology . Oct2008, Vol. 295, pF1063-F1070. 8p. 5 Graphs. - Publication Year :
- 2008
-
Abstract
- 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 mm. 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. [ABSTRACT FROM AUTHOR]
- Subjects :
- *ELECTROPHYSIOLOGY
*ENDOTHELINS
*PHOSPHOLIPASE C
*TYROSINE
*PROTEIN-tyrosine kinases
Subjects
Details
- Language :
- English
- ISSN :
- 1931857X
- Volume :
- 295
- Database :
- Academic Search Index
- Journal :
- American Journal of Physiology: Renal Physiology
- Publication Type :
- Academic Journal
- Accession number :
- 35008807
- Full Text :
- https://doi.org/10.1152/ajprenal.90321.2008