Skip Navigation

Cardiovascular Research 2001 52(3):487-499; doi:10.1016/S0008-6363(01)00412-6
© 2001 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Fransen, P.
Right arrow Articles by Sys, S. U
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Fransen, P.
Right arrow Articles by Sys, S. U
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2001, European Society of Cardiology

Distribution and role of Na+/K+ ATPase in endocardial endothelium

Paul Fransen*, Jan Hendrickx, Dirk L Brutsaert and Stanislas U Sys

Department of Physiology and Medicine, University of Antwerp (RUCA), Groenenborgerlaan, 171, B-2020 Antwerp, Belgium

* Corresponding author. Tel.: +32-3-218-0278; fax: +32-3-218-0276 fransen{at}ruca.ua.ac.be

Objective: In mammalian cardiomyocytes, {alpha} isoforms of Na+/K+ ATPase have specific localisation and function, but their role in endocardial endothelium is unknown. Methods: Different {alpha} isoforms in endocardial endothelium and cardiomyocytes of rabbit were investigated by measuring contractile parameters of papillary muscles, by RT-PCR, by Western blots and by immunocytochemistry. Results: Inhibition of Na+/K+ ATPase by decreasing external K+ from 5.0 to 0.5 mmol/l caused biphasic inotropic effects. The maximal negative inotropic effect at external K+ of 2.5 mmol/l was significantly larger in +EE muscles (with intact endocardial endothelium) than in -EE muscles (with endocardial endothelium removed) (–22.5±2.4% versus –5.9±4.0%, n=7, P<0.05). Further decrease of K+ to 0.5 mmol/l caused endothelium-independent positive inotropy (27.8±11.8% for +EE versus 18.6±11.3% for –EE, n=7, P>0.05). Inhibition of Na+/K+ ATPase either by dihydro-ouabain (10–9 to 10–4 mol/l, n=4) or by K+ decrease following inhibition of Na+–H+ exchanger by dimethyl-amiloride (50 µmol/l, n=6) caused endothelium-independent positive inotropic effects only. RT-PCR and Western Blot demonstrated {alpha}1 and {alpha}2 Na-K-ATPase isoforms in cardiomyocytes, but only {alpha}1 in cultured endocardial endothelial cells. Immunohistochemistry showed that {alpha}1 in endocardial endothelium was predominantly present at the luminal side of the cell (n=7) and that {alpha}1 and {alpha}2 displayed different localisation in cardiomyocytes. Conclusions: These results suggested that negative and positive inotropic effects of Na+/K+ ATPase inhibition in +EE muscles could be attributed to inhibition of endocardial endothelial {alpha}1 and muscle {alpha}2 isoform, respectively. Accordingly, the endocardial endothelial {alpha}1 isoform of Na+/K+ ATPase may contribute to blood–heart barrier properties of this endothelium and may control cardiac performance via endothelial Na+/H+ exchange.

KEYWORDS PECAM: platelet endothelial cell adhesion molecule; P: polyclonal antibody; M: monoclonal antibody; NCE: Na+/Ca2+ exchanger; NHE: Na+/H+ exchanger; UB: Upstate Biotechnology; ABR: Affinity Biotechnology Reagents


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
F. Swift, N. Tovsrud, U. H. Enger, I. Sjaastad, and O. M. Sejersted
The Na+/K+-ATPase {alpha}2-isoform regulates cardiac contractility in rat cardiomyocytes
Cardiovasc Res, July 1, 2007; 75(1): 109 - 117.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
K. Lemmens, V. F. M. Segers, M. Demolder, and G. W. De Keulenaer
Role of Neuregulin-1/ErbB2 Signaling in Endothelium-Cardiomyocyte Cross-talk
J. Biol. Chem., July 14, 2006; 281(28): 19469 - 19477.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
P. Fransen
Phospholemman, a chaperone of Na+,K+-ATPase?
Cardiovasc Res, January 1, 2005; 65(1): 13 - 15.
[Full Text] [PDF]

Home page
 Physiol. GenomicsHome page
J. Hendrickx, K. Doggen, E. O. Weinberg, P. Van Tongelen, P. Fransen, and G. W. De Keulenaer
Molecular diversity of cardiac endothelial cells in vitro and in vivo
Physiol Genomics, October 4, 2004; 19(2): 198 - 206.
[Abstract] [Full Text] [PDF]

Home page
 Cardiovasc ResHome page
P. Fransen, R. R Lamberts, J. Hendrickx, and G. W De Keulenaer
Endocardial endothelium modulates subendocardial pHi of rabbit papillary muscles: role of transendothelial HCO3- transport
Cardiovasc Res, September 1, 2004; 63(4): 700 - 708.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
K. Lemmens, P. Fransen, S. U. Sys, D. L. Brutsaert, and G. W. De Keulenaer
Neuregulin-1 Induces a Negative Inotropic Effect in Cardiac Muscle: Role of Nitric Oxide Synthase
Circulation, January 27, 2004; 109(3): 324 - 326.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
D. L. Brutsaert
Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity
Physiol Rev, January 1, 2003; 83(1): 59 - 115.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.