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Cardiovascular Research Advance Access first published online on October 22, 2008
This version [Corrected Proof] published online on November 14, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn285
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.

Sarcolemmal Ca2+-ATPase ability to transport Ca2+ gradually diminishes after myocardial infarction in the rat

Urszula Mackiewicz1,*, Michal Maczewski1, Anna Konior1, James O. Tellez2, Dominika Nowis3, Halina Dobrzynski2, Mark R. Boyett2 and Bohdan Lewartowski1

1 Department of Clinical Physiology, Postgraduate Medical School, Marymoncka Str 99/101, 01-813 Warsaw, Poland
2 Cardiovascular Research Group, University of Manchester, Manchester, UK
3 Department of Immunology, Center of Biostructure Research, Medical University of Warsaw, Warsaw, Poland

* Corresponding author. Tel: +48 225693840; fax: +48 225693712. E-mail address: urszulam{at}cmkp.edu.pl

Aims: Plasmalemmal Ca2+-ATPase (PMCA) is involved in Ca2+ handling and the regulation of intracellular signalling pathways in the heart. However, there is no information on its functioning in heart hypertrophy and failure. We aimed to investigate the Ca2+-transporting ability of PMCA, Na+/Ca2+ exchanger (NCX), and sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a), as well as the amplitude of Ca2+ transients and cell shortening in myocytes isolated from rat hearts at various time intervals after myocardial infarction (MI).

Methods and results: The rate of Ca2+ transport by PMCA, NCX, and SERCA2a was estimated from the rate constants of decay of electrically and caffeine-evoked Ca2+ transients in left ventricular myocytes isolated 1 week, 1 month, and 3 months after MI. One week, 1 month, and 3 months after MI, the transporting function of PMCA decreased by 27, 41, and 67%, respectively, compared with that in time-matched sham animals. This was accompanied by increased amplitude of Ca2+ transients, cell shortening, and SR Ca2+ content. Carboxyeosin, a blocker of PMCA, increased the amplitude of shortening in cells extracted from control hearts. This effect was absent 1 and 3 months after MI. PMCA1, 2, and 4 mRNAs were unchanged in the ventricular muscle 3 months after MI when compared with time-matched sham animals. The transporting function of NCX was increased by 65% only 3 months after MI, whereas that of SERCA2a was decreased by ~18% at all three time points after MI.

Conclusion: The ability of PMCA to transport Ca2+ progressively decreases over 3 months after MI. This decrease may contribute to the increase in amplitude of Ca2+ transients and myocyte shortening.

KEYWORDS Sarcolemmal Ca2+-ATPase; Calcium handling; Myocardial infarction; Heart remodelling

Time for primary review: 28 days


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