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Cardiovascular Research 2001 52(3):487-499; doi:10.1016/S0008-6363(01)00412-6
© 2001 by European Society of Cardiology
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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


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