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(The FASEB Journal. 2008;22:lb635)
© 2008 FASEB
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lb635

The Na+/Ca2+ exchange inhibitor SEA0400 fails to enhance cytosolic Ca2+ transient and contractility in isolated canine ventricular myocytes

Andras Toth1, Peter Birinyi2, Karoly Acsai1, Norbert Nagy1, Janos Prorok1, Norbert Szentandrassy2, Janos Magyar2, Peter P. Nanasi2, Julius Gy. Papp1 and Andras Varro1

1 Pharmacology and Pharmacotherapy, University of Szeged, Szeged, Hungary,
2 Physiology, University of Debrecen, Debrecen, Hungary

ABSTRACT

This study was designed to evaluate the effects of the Na+/Ca2+ exchange (NCX) inhibitor, SEA0400 on Ca2+ handling in isolated canine ventricular myocytes. Intracellular Ca2+ ([Ca2+]i) transients, induced by field stimulation or caffeine flush, were monitored using Ca2+ indicator dyes. [Ca2+]i-dependent modulation of the inhibitory effect of SEA0400 on NCX was characterized by the changes in Ni2+ sensitive current in voltage clamped myocytes. In myocytes paced at 1 Hz, neither diastolic [Ca2+]i, nor the amplitude of [Ca2+]i transients were significantly altered by SEA0400 up to the concentration of 1 µM. The blocking effect of SEA0400 on NCX decreased with increasing [Ca2+]i, and it was more pronounced in reverse than in forward mode. The rate of decay of the caffeine-induced [Ca2+]i transients, was decreased significantly by 1 µM SEA0400, however, this effect was only a fraction of that observed with 10 mM NiCl2. The lack of any major SEA0400-induced shift in Ca2+ transients or contractility of myocytes can well be explained by its limited inhibitory effect on NCX further attenuated by elevated [Ca2+]i levels and a concomitant reduction in Ca2+ influx due to the predominantly reverse mode blockade of NCX. Support: Hungarian: NKFP-1A/046/2004; OTKA-K68457, OTKA-K73160, OTKA-NI61902, OTKA-K61442 ETT-060/2006, ETT-449/2006, European Community: LSHM-CT-2005-018833, LSHM-CT-2005-018676





This Article
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