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Cardiovascular Research 1997 34(1):99-103; doi:10.1016/S0008-6363(97)00006-0
© 1997 by European Society of Cardiology
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Copyright © 1997, European Society of Cardiology

Cytosolic Ca2+ concentration decreases in diabetic rat myocytes

Hideharu Hayashia,* and Naohisa Nodab

aPhoton Medical Research Center, Hamamatsu University School of Medicine, 3600 Handa-cho, Hamamatsu 431-31, Japan
bThird Department of Internal Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan

* Corresponding author. Tel. +81 53 435-2391; Fax +81 53 435-2394.

Received 17 September 1996; accepted 13 December 1996

KEYWORDS Diabetes, cardiomyopathy; Calcium, intracellular concentration; Sodium, intracellular concentration; Calcium transient; Contractile function

The first 150 words of the full text of this article appear below.

Diabetes mellitus has been shown to be associated with heart failure of unknown origin, which is termed ‘diabetic cardiomyopathy’ [1]. Regan et al. [2]have shown that the small vessel lesions in diabetes mellitus have little or no relation to diabetic cardiomyopathy, suggesting that the contractile function of the diabetic cardiomyopathy was primarily defective. Although many studies have been performed to reveal cellular and subcellular derangement in diabetic cardiomyopathy [3–6], the precise mechanism is still unknown.

It has been reported that Ca2+ metabolism in diabetic myocardium has several abnormalities, including a decreased activity of Ca2+-ATPase in sarcoplasmic reticulum (SR) [7, 8]and sarcolemma [9, 10]. It has also been reported that the activity of Na+/Ca2+ exchange is lower in diabetic myocardium [10]. These reports have suggested that Ca2+ overload may be involved in the pathogenesis of diabetic cardiomyopathy [3]. Although it has been . . . [Full Text of this Article]


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