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Research Article Free access | 10.1172/JCI114611

Role of intracellular calcium handling in force-interval relationships of human ventricular myocardium.

J K Gwathmey, M T Slawsky, R J Hajjar, G M Briggs, and J P Morgan

Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts 02215.

Find articles by Gwathmey, J. in: PubMed | Google Scholar

Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts 02215.

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Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts 02215.

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Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts 02215.

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Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts 02215.

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Published May 1, 1990 - More info

Published in Volume 85, Issue 5 on May 1, 1990
J Clin Invest. 1990;85(5):1599–1613. https://doi.org/10.1172/JCI114611.
© 1990 The American Society for Clinical Investigation
Published May 1, 1990 - Version history
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Abstract

Experiments were performed in human working myocardium to investigate the relationship of intracellular calcium handling and availability to alterations in the strength of contraction produced by changes in stimulation rate and pattern. Both control and myopathic muscles exhibited potentiation of peak isometric force during the postextrasystolic contraction which was associated with an increase in the peak intracellular calcium transient. Frequency-related force potentiation was attenuated in myopathic muscles compared to controls. This occurred despite an increase in resting intracellular calcium and in the peak amplitude of the calcium transient as detected with aequorin. Therefore, abnormalities in contractile function of myopathic muscles during frequency-related force potentiation are not due to decreased availability of intracellular calcium, but more likely reflect differences in myofibrillar calcium responsiveness. Sarcolemmal calcium influx may also contribute to frequency-related changes in contractile force in myopathic muscles as suggested by a decrease in action potential duration with increasing stimulation frequency which is associated with fluctuations in peak calcium transient amplitude.

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