Am J Physiol Cell Physiol AJP: Renal Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 264: C352-C360, 1993;
0363-6143/93 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
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 HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ohara, A.
Right arrow Articles by Eaton, D. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ohara, A.
Right arrow Articles by Eaton, D. C.

AJP - Cell Physiology, Vol 264, Issue 2 C352-C360, Copyright © 1993 by American Physiological Society

ARTICLES

G protein activation inhibits amiloride-blockable highly selective sodium channels in A6 cells

A. Ohara, H. Matsunaga and D. C. Eaton
Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322.

Single-channel methods were used to examine the regulation of amiloride-blockable highly selective sodium channels by guanine nucleotide-binding proteins (G proteins). A6 cells (a renal cell line derived from Xenopus laevis kidney) were cultured on permeable collagen films, and patch recordings were made from the apical membranes of confluent cells. The predominant channel in the apical membranes is a highly selective, 4-pS, amiloride-blockable sodium channel (the Na(+)-to-K+ permeability ratio is > 30). In inside-out patches, application to the cytosolic surface of guanosine-5'-O-(2-thiodiphosphate) (GDP beta S), which deactivates G proteins, increased sodium channel activity. GDP beta S produced a sevenfold increase in channel activity. In contrast, GTP and guanosine-5'-O-(3-thiotriphosphate) (GTP gamma S) decreased sodium channel activity to about one-twentieth of the untreated value. The effect of GTP (but not GTP gamma S) was reversible. In cell-attached patches, a 3- to 4-h exposure of the apical membrane to pertussis toxin (PTX) increased the mean open time of sodium channels approximately 2.7 times and the open probability approximately 1.6-fold, but pretreatment of apical membranes with cholera toxin (250 ng/ml) for 3-4 h had no effect on open probability or mean open time. These results imply that a PTX-sensitive G protein regulates amiloride-blockable highly selective sodium channels in the apical membranes of A6 cells and that the G protein in a GTP-bound, activated state inhibits sodium channel activity.


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
S. Matalon, A. Lazrak, L. Jain, and D. C. Eaton
Lung Edema Clearance: 20 Years of Progress: Invited Review: Biophysical properties of sodium channels in lung alveolar epithelial cells
J Appl Physiol, November 1, 2002; 93(5): 1852 - 1859.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
R. S. Edinger, M. D. Rokaw, and J. P. Johnson
Vasopressin stimulates sodium transport in A6 cells via a phosphatidylinositide 3-kinase-dependent pathway
Am J Physiol Renal Physiol, October 1, 1999; 277(4): F575 - F579.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
S. Sariban-Sohraby, M. Svoboda, and F. Mies
Guanine nucleotide binding proteins in cultured renal epithelia: studies with pertussis toxin and aldosterone
Am J Physiol Renal Physiol, January 1, 1999; 276(1): F10 - F17.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
R. A. Shimkets, R. Lifton, and C. M. Canessa
In vivo phosphorylation of the epithelial sodium channel
PNAS, March 17, 1998; 95(6): 3301 - 3305.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online