AJP - Renal AJP: Gastrointestinal and Liver Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol 249: F160-F168, 1985;
0363-6127/85 $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 Gullans, S. R.
Right arrow Articles by Shulman, R. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gullans, S. R.
Right arrow Articles by Shulman, R. G.

AJP - Renal Physiology, Vol 249, Issue 1 160-F168, Copyright © 1985 by American Physiological Society

ARTICLES

NMR measurements of intracellular sodium in the rabbit proximal tubule

S. R. Gullans, M. J. Avison, T. Ogino, G. Giebisch and R. G. Shulman

The present study evaluated the use of nuclear magnetic resonance (NMR) spectroscopy to monitor directly and continuously intracellular sodium levels in rabbit renal cortical tubule suspensions. When the paramagnetic shift reagent dysprosium tripolyphosphate was added to the extracellular medium it was possible to resolve signals from intracellular and extracellular sodium without adversely affecting cellular viability. An efflux of intracellular sodium against a significant concentration gradient was observed when sodium-loaded cells were warmed from 4 to 37 degrees C. At 37 degrees C in steady state, inhibition of Na+-K+-ATPase activity by ouabain increased intracellular sodium content in a dose-dependent and time-dependent manner. A biphasic time course of increased intracellular sodium following ouabain (10(-3) M) suggested that the sodium permeability of the plasma membrane may decrease following pump inhibition, thus limiting sodium influx. Nystatin, an agent known to facilitate sodium entry across cell membranes, increased intracellular sodium fivefold. In another series of experiments several maneuvers were performed to ascertain the fraction of intracellular sodium that was NMR visible. Quantitative assessment of either an efflux or influx of sodium indicated that the NMR visibility of the transported sodium was 100%. Furthermore, disruption of the cell membranes with Triton X-100 showed that the entire pool of intracellular sodium was 100% NMR visible.(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
M. J. Morton, S. Chipperfield, A. Abohamed, A. Sivaprasadarao, and M. Hunter
Na+-induced inward rectification in the two-pore domain K+ channel, TASK-2
Am J Physiol Renal Physiol, January 1, 2005; 288(1): F162 - F169.
[Abstract] [Full Text] [PDF]


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