AJP - Renal Watch the video to see how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol 295: F1063-F1070, 2008. First published July 30, 2008; doi:10.1152/ajprenal.90321.2008
0363-6127/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplemental Figure
Right arrow All Versions of this Article:
295/4/F1063    most recent
90321.2008v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bugaj, V.
Right arrow Articles by Stockand, J. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bugaj, V.
Right arrow Articles by Stockand, J. D.

Regulation of the epithelial Na+ channel by endothelin-1 in rat collecting duct

Vladislav Bugaj,1 Oleh Pochynyuk,1 Elena Mironova,1 Alain Vandewalle,2 Jorge L. Medina,1 and James D. Stockand1

1Department of Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas; and 2Institut National de la Santé et de la Recherche Médicale U773, Centre de Recherche Biomedicale Bichat-Beaujon and Universite Paris, Paris, France

Submitted 19 May 2008 ; accepted in final form 24 July 2008

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.

salt-sensitive hypertension; systemic blood pressure


Address for reprint requests and other correspondence: O. Pochynyuk, Dept. of Physiology 7756, Univ. of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900 (e-mail: pochynyuk{at}uthscsa.edu)






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.