© 1996 by European Society of Cardiology
Copyright © 1996, European Society of Cardiology
Cardiac Na+/Ca2+ exchange activity in patients with end-stage heart failure
aUniversitätsklinik Freiburg, Innere Medizin III, Kardiologie und Angiologie, Breisacher Str. 33, 79106 Freiburg, Germany
bMax-Delbrück-Zentrum für Molekulare Medizin, Berlin-Buch, Germany
cUniversität Halle, Institut für Pathophysiologie, Halle, Germany
* Corresponding author. Tel. (+49-761) 270-7009; Fax (+49-761) 270-7041. reinecke{at}sun2.ruf.uni-freiburg.de
Objective: The aim of the present study was to investigate the functional activity and expression of the sarcolemmal Na+/Ca2+ -exchanger in the failing human heart. Methods: Left ventricular samples were taken from eleven patients with end-stage heart failure and six organ donors (normal controls). The Na+/Ca2+-exchanger activity was assessed by measuring Na+ gradient-induced 45Ca2+ transport into sarcolemmal vesicles of quantitatively collected crude membrane preparations. The abundance of the Na+/Ca2+-exchanger protein was determined by Western blot analysis using a specific antiserum and the results were normalized to myocyte specific β-myosin heavy chain protein content. Results: In membrane preparations of failing human hearts, both the Na+ gradient-induced 45Ca2+ transport activity and the level of immunoreactive Na+/Ca2+-exchanger protein were increased (P < 0.01) by 87% and 160% compared to controls, respectively. Conclusions: In human end-stage heart failure the increased sarcolemmal Na+/Ca2+-exchanger activity appears to be due to an elevated expression of this protein. An increase in the expression and activity of the Na+/Ca2+-exchanger in the failing human heart may be of important functional significance: while a resulting increase in Ca2+ extrusion across the sarcolemma may limit diastolic Ca2+ overload, a corresponding influx of Na+ may be associated with membrane depolarization and enhanced arrhythmogenesis if the Na+Ca2+-exchanger operates primarily in the forward mode.
KEYWORDS Na+/Ca2+-exchange; Calcium fluxes; Heart failure; Human, ventricle
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