J Physiol Society Membership
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Physiol Vol 480, Issue Pt 1 pp 9-20
Copyright © 1994 by The Physiological Society
This Article
Right arrow Full Text (PDF)
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 Doering, A E
Right arrow Articles by Lederer, W J
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Doering, A E
Right arrow Articles by Lederer, W J

The action of Na+ as a cofactor in the inhibition by cytoplasmic protons of the cardiac Na(+)-Ca2+ exchanger in the guinea-pig.

 A E Doering and W J Lederer

Department of Physiology, University of Maryland School of Medicine, Baltimore 21201.

1. Na(+)-Ca2+ exchange current was activated in giant excised patches of guinea-pig cardiac sarcolemma by raising the intracellular sodium concentration ([Na+]i). When the pHi was simultaneously acidified to 6.4, the current was transient, dropping by 80% in 30 s. 2. Pre-exposure to a pHi of 6.4 for 15 s reduced the peak Na(+)-Ca2+ exchange current without altering the decay rate or steady-state current. Recovery from proton inhibition was seen when [Na+]i was removed for 9 s. 3. A mathematical model of Na(+)-Ca2+ exchange function reproduced the experimental results. In addition, two model-dependent predictions were seen experimentally. (i) [Na+]i-dependent 'inactivation' of Na(+)-Ca2+ exchange may arise from pHi effects. We observed experimentally that pre-exposure to acidic pHi can remove the transient current component attributed to [Na+]i-dependent 'inactivation'. (ii) self-exchange should be inhibited by acidification. This has been observed by other investigators. 4. We have hypothesized that there are two components to inhibition of the Na(+)-Ca2+ exchanger by intracellular protons, and that one is enhanced by increased [Na+]i (Doering & Lederer, 1993b). This hypothesis is supported by the data presented here and by a model of Na(+)-Ca2+ exchange behaviour in which binding of intracellular sodium to the exchanger enhances the affinity of the exchanger for inhibitory intracellular protons.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
O. Chernysh, M. Condrescu, and J. P. Reeves
Sodium-dependent inactivation of sodium/calcium exchange in transfected Chinese hamster ovary cells
Am J Physiol Cell Physiol, October 1, 2008; 295(4): C872 - C882.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
L. Beauge and R. DiPolo
Dual effect of Nai+ on Ca2+ influx through the Na+/Ca2+ exchanger in dialyzed squid axons. Experimental data confirming the validity of the squid axon kinetic model
Am J Physiol Cell Physiol, January 1, 2008; 294(1): C118 - C125.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
R. Dipolo and L. Beauge
Sodium/Calcium Exchanger: Influence of Metabolic Regulation on Ion Carrier Interactions
Physiol Rev, January 1, 2006; 86(1): 155 - 203.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
L. Beauge and R. DiPolo
SEA-0400, a potent inhibitor of the Na+/Ca2+ exchanger, as a tool to study exchanger ionic and metabolic regulation
Am J Physiol Cell Physiol, June 1, 2005; 288(6): C1374 - C1380.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1994 The Physiological Society.