AJP - Renal AJP: Lung Cellular and Molecular Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol 252: F661-F669, 1987;
0363-6127/87 $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 Melton, J. E.
Right arrow Articles by Cserr, H. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Melton, J. E.
Right arrow Articles by Cserr, H. F.

AJP - Renal Physiology, Vol 252, Issue 4 661-F669, Copyright © 1987 by American Physiological Society

ARTICLES

Volume regulatory loss of Na, Cl, and K from rat brain during acute hyponatremia

J. E. Melton, C. S. Patlak, K. D. Pettigrew and H. F. Cserr

This study quantitatively evaluates the contribution of tissue Na, Cl, and K loss to brain volume regulation during acute dilutional hyponatremia (DH) and examines the mechanism of Na loss. DH was produced in pentobarbital sodium-anesthetized rats by intraperitoneal infusion of distilled water and brain water and electrolytes analyzed 30 min, 1 h, 3 h, 4 h, or 6 h later. The rate of Na and Cl loss was greatest during the first 30 min of DH (0.43 and 0.47 meq X kg tissue dry wt-1 X min-1, respectively). Net loss of Na and Cl was maximal after 3 h of DH. K loss was slower, achieving significance after 3 h. Electrolyte loss was sufficient to account for observed brain volume regulation after three or more hours of DH. Measurements of 22Na influx and efflux across the blood-brain barrier showed that barrier permeability to Na is unchanged during DH. Analysis of results using a two-compartment model of plasma-brain exchange suggests that loss of brain Na during DH does not result solely from a shift of electrolyte across the blood-brain barrier to plasma, and thus provides indirect evidence for an additional pathway for Na loss, presumably via cerebrospinal fluid.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
J. C. Ayus, S. G. Achinger, and A. Arieff
Brain cell volume regulation in hyponatremia: role of sex, age, vasopressin, and hypoxia
Am J Physiol Renal Physiol, September 1, 2008; 295(3): F619 - F624.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
D. J. Foster, A. M. Heacock, R. F. Keep, and S. K. Fisher
Activation of Muscarinic Cholinergic Receptors on Human SH-SY5Y Neuroblastoma Cells Enhances Both the Influx and Efflux of K+ under Conditions of Hypo-Osmolarity
J. Pharmacol. Exp. Ther., May 1, 2008; 325(2): 457 - 465.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
S. M. Silver, B. M. Schroeder, P. Bernstein, and R. H. Sterns
Brain adaptation to acute hyponatremia in young rats
Am J Physiol Regulatory Integrative Comp Physiol, June 1, 1999; 276(6): R1595 - R1599.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
F. LANG, G. L. BUSCH, M. RITTER, H. VOLKL, S. WALDEGGER, E. GULBINS, and D. HAUSSINGER
Functional Significance of Cell Volume Regulatory Mechanisms
Physiol Rev, January 1, 1998; 78(1): 247 - 306.
[Abstract] [Full Text] [PDF]


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