Cardiac Na+/Ca2+ exchange activity in patients with end-stage heart failure

Item Type:	Article
Title:	Cardiac Na+/Ca2+ exchange activity in patients with end-stage heart failure
Creators Name:	Reinecke, H. and Studer, R. and Vetter, R. and Holtz, J. and Drexler, H.
Abstract:	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 beta-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, Ventricle Human
Source:	Cardiovascular Research
ISSN:	0008-6363
Publisher:	Elsevier
Volume:	31
Number:	1
Page Range:	48-54
Date:	1 January 1996
Official Publication:	https://doi.org/10.1016/S0008-6363(95)00176-X
PubMed:	View item in PubMed

Repository Staff Only: item control page