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: F346-F356, 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 Pritchard, J. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Pritchard, J. B.

AJP - Renal Physiology, Vol 252, Issue 2 346-F356, Copyright © 1987 by American Physiological Society

ARTICLES

Sulfate-bicarbonate exchange in brush-border membranes from rat renal cortex

J. B. Pritchard

Under Na+-free conditions, SO4(2-) uptake by rat renal brush-border membrane (BBM) vesicles could be driven by imposition of a HCO3- gradient (in greater than out). The initial rate of SO4(2-) uptake was stimulated 10-fold, and peak overshoot exceeded equilibrium uptake by 2-3 times. Cl-, SCN-, NO3-, I-, and OH- were able to substitute for HCO3-. Divalent anions, including SO4(2-) itself, were less effective as counterions. Similarly, in the absence of Na+,SO4(2-) efflux was stimulated most effectively by the monovalent ions. HCO3- -SO4(2-) exchange was cis-inhibited by disulfonic stilbenes [4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS), 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)], phloretin, Hg, and S2O3(2-). HCO3- driven SO4(2-) uptake was saturable, with an apparent Km of 0.4 mM for SO4(2-). Simultaneous imposition of Na+ (out greater than in) and HCO3- (in greater than out) gradients produced approximately additive stimulation of SO4(2-) uptake. The HCO3- -driven component of SO4(2-) uptake, but not the component driven by Na+, was inhibited by SITS. Finally, Na+-driven SO4(2-) accumulation could be reduced by imposing an out greater than in HCO3- gradient, conditions accelerating exchange driven SO4(2-) efflux. These findings indicate the presence of separate Na+-SO4(2-) cotransport and SO4(2-)-anion exchange pathways in the same BBM vesicles.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
R. M. Pelis and J. L. Renfro
Role of tubular secretion and carbonic anhydrase in vertebrate renal sulfate excretion
Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2004; 287(3): R491 - R501.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
D. Markovich
Physiological Roles and Regulation of Mammalian Sulfate Transporters
Physiol Rev, October 1, 2001; 81(4): 1499 - 1533.
[Abstract] [Full Text] [PDF]

Home page
 J. Pharmacol. Exp. Ther.Home page
K. Sagawa, I. M. Darling, H. Murer, and M. E. Morris
Glucocorticoid-Induced Alterations of Renal Sulfate Transport
J. Pharmacol. Exp. Ther., August 1, 2000; 294(2): 658 - 663.
[Abstract] [Full Text]

Home page
 Am. J. Physiol. Renal Physiol.Home page
L. P. Karniski
Effects of sulfate and chloride on three separate oxalate transporters reconstituted from rabbit renal cortex
Am J Physiol Renal Physiol, January 1, 1998; 274(1): F189 - F196.
[Abstract] [Full Text] [PDF]


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