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Am J Physiol Heart Circ Physiol 279: H2259-H2268, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 5, H2259-H2268, November 2000

Characterization of nifedipine-resistant calcium current in neonatal rat ventricular cardiomyocytes

Christophe Pignier and Daniel Potreau

Centre National de la Recherche Scientifique, UMR 6558, Laboratoire des Biomembranes et Signalisation Cellulaire, Faculty of Sciences, University of Poitiers, 86022 Poitiers cedex, France

Calcium current was recorded from ventricular cardiomyocytes of rats at various stages of postnatal development using the whole cell patch-clamp technique. In cultured 3-day-old neonatal cells, the current carried by Ca2+ or Ba2+ (5 mM) was not completely inhibited by 2 µM nifedipine. A residual current was activated in the same voltage range as the L-type, nifedipine-sensitive Ca2+ current, but its steady-state inactivation was negatively shifted by 16 mV. This nifedipine-resistant calcium current was not further inhibited by other organic calcium current antagonists such as PN200-110, verapamil, and diltiazem nor by nickel, omega -conotoxin, or tetrodotoxin. It was completely blocked by cadmium and increased by isoproterenol and forskolin. This current was >20% of total calcium current in ventricular myocytes freshly isolated from neonatal rats, and it decreased during postnatal maturation, disappearing at the adult stage. This suggests that this current could be caused by an isoform of the L-type calcium channel expressed in a way that reflects the developmental stage of the rat heart.

rats; heart; development; Ca2+ channel isoform


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