Activation of Ca-permeable cation channels by myocarditis-associated antibody in guinea pig ventricular myocytes.

M Tominaga; A Matsumori; M Horie; H Yoshida; Y Okada

doi:10.1172/JCI116285

Third Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.

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Third Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.

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Third Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.

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Third Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.

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Third Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.

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Published in Volume 91, Issue 3 on March 1, 1993
J Clin Invest. 1993;91(3):1231–1234. https://doi.org/10.1172/JCI116285.
© 1993 The American Society for Clinical Investigation

Published March 1, 1993 - Version history

The pathogenesis of myocarditis and dilated cardiomyopathy is though to involve autoimmunological processes and myocardial calcium overload. Serum containing antiheart antibodies associated with a murine model of myocarditis increased [Ca2+]i in guinea pig ventricular myocytes only in the presence of extracellular Ca2+. The antiheart antibody-positive serum activated Ca(2+)-permeable cation channels that were insensitive to dihydropyridines and membrane stretch. The permeability sequence was Ba2+ > Ca2+ > Na+ approximately K+, and the single-channel conductance to Ba2+ was 12 pS. The channel was activated by extracellular application of the serum during on-cell recording, which suggests that a soluble intracellular messenger may be involved. The antibody-positive serum did not alter voltage-gated Ca2+ currents. We propose that excess Ca entry in myocarditis and dilated cardiomyopathy results from activation of a Ca(2+)-permeable cationic channel by the autoantibodies.

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