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January 1, 1998AJP Heart and Circulatory Physiology

Alterations in cardiac SR Ca2+-release channels during development of heart failure in cardiomyopathic hamsters

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Authors

TUTakeshi UeyamaYamaguchi Prefecture Central Hospital TOTomoko OhkusaUbe Frontier University YHYuji HisamatsuToho University

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Implication

RyR changes track hamster HF progression; leaves open whether similar dynamics drive human Ca2+ dysregulation.

Key Points

Key points are not available for this paper at this time.

Cite This Study

Ueyama et al. (1998) studied this question.

synapsesocial.com/papers/6a8bdcab52e1a91077e98119 https://doi.org/10.1152/ajpheart.1998.274.1.h1

Topics

Heart failure HFrEF treatment Echocardiography Cardiomyopathy Cardiac amyloidosis

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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

1Calcium transport properties of cardiac sarcoplasmic reticulum from cardiomyopathic Syrian hamsters (BIO 53.58 and 14.6): evidence for a quantitative defect in dilated myopathic hearts not evident in hypertrophic hearts.1988 · 91 citations
2Increased mechanical extraction of T-tubule/junctional SR from cardiomyopathic hamster heart1993 · 12 citations
3Cardiomyopathic and healthy acidotic hamster hearts: mitochondrial activity may regulate cardiac performance1986 · 41 citations
4Improvement in myocardial performance without a decrease in high-energy phosphate metabolites after isoproterenol in Syrian cardiomyopathic hamsters.1988 · 35 citations
5Decrease in myocardial ryanodine receptors and altered excitation-contraction coupling early in the development of heart failure.1994 · 107 citations