AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 272: H606-H612, 1997;
0363-6135/97 $5.00
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AJP - Heart and Circulatory Physiology, Vol 272, Issue 2 606-H612, Copyright © 1997 by American Physiological Society

ARTICLES

Phospholamban deficiency alters inactivation kinetics of L-type Ca2+ channels in mouse ventricular myocytes

H. Masaki, Y. Sato, W. Luo, E. G. Kranias and A. Yatani
Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Ohio 45267, USA.

Entry of Ca2+ through voltage-dependent L-type Ca2+ channels is critical for contraction in cardiac cells. In recent studies, cells from phospholamban (PLB) knockout (PLB-KO) mouse hearts showed significantly increased basal contractility with enhanced sarcoplasmic reticulum (SR) Ca2+ uptake. To test whether these effects of PLB ablation were associated with alterations of L-type Ca2+ channel function, we compared the properties of Ca2+ channel currents (I(Ca)) in ventricular myocytes isolated from wild-type (WT) and PLB-KO mouse hearts. L-type Ca2+ channels from mouse myocytes exhibited voltage-dependent gating and sensitivity to dihydropyridine drugs, similar to other mammalian species, and these properties were not altered by PLB ablation. I(Ca) from both WT and PLB-KO cells revealed two (fast and slow) components of inactivation kinetics. However, the proportion of the faster component was significantly larger in PLB-KO cells. Ryanodine (10 microM) reduced the rate of inactivation of I(Ca) for both WT and PLB-KO cells, but the reduction was more prominent in PLB-KO cells compared with WT cells. In contrast, the inactivation in a Ba2+ solution could be fitted by a single exponential similar to the slower component in Ca2+, and this was not altered in PLB-KO cells. The increase in the fast Ca2+-dependent inactivation component in PLB-KO cells supports the hypothesis that Ca2+ released from the SR regulates Ca2+ channel inactivation by affecting the levels of Ca2+ near the channel and suggests that this may be an important compensatory mechanism in the hyperdynamic PLB-KO heart.


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