AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 283: H1398-H1408, 2002. First published June 27, 2002; doi:10.1152/ajpheart.00313.2002
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Vol. 283, Issue 4, H1398-H1408, October 2002

Defective intracellular Ca2+ signaling contributes to cardiomyopathy in Type 1 diabetic rats

Kin M. Choi1, Yan Zhong1, Brian D. Hoit2,3, Ingrid L. Grupp1, Harvey Hahn2, Keith W. Dilly4, Silvia Guatimosim4, W. Jonathan Lederer4, and Mohammed A. Matlib1

1 Departments of Pharmacology and Cell Biophysics and 2 Internal Medicine (Division of Cardiology), University of Cincinnati, Cincinnati 45267; 3 Department of Medicine, Case Western Reserve University, Cleveland, Ohio 44106; and 4 Medical Biotechnology Center and Department of Physiology, University of Maryland, Baltimore, Maryland 21201

The goal of the study was to determine whether defects in intracellular Ca2+ signaling contribute to cardiomyopathy in streptozotocin (STZ)-induced diabetic rats. Depression in cardiac systolic and diastolic function was traced from live diabetic rats to isolated individual myocytes. The depression in contraction and relaxation in myocytes was found in parallel with depression in the rise and decline of intracellular free Ca2+ concentration ([Ca2+]i). The sarcoplasmic reticulum (SR) Ca2+ store and rates of Ca2+ release and resequestration into SR were depressed in diabetic rat myocytes. The rate of Ca2+ efflux via sarcolemmal Na+/Ca2+ exchanger was also depressed. However, there was no change in the voltage-dependent L-type Ca2+ channel current that triggers Ca2+ release from the SR. The depression in SR function was associated with decreased SR Ca2+-ATPase and ryanodine receptor proteins and increased total and nonphosphorylated phospholamban proteins. The depression of Na+/Ca2+ exchanger activity was associated with a decrease in its protein level. Thus it is concluded that defects in intracellular Ca2+ signaling caused by alteration of expression and function of the proteins that regulate [Ca2+]i contribute to cardiomyopathy in STZ-induced diabetic rats. The increase in phospholamban, decrease in Na+/Ca2+ exchanger, and unchanged L-type Ca2+ channel activity in this model of diabetic cardiomyopathy are distinct from other types of cardiomyopathy.

myocytes; sarcoplasmic reticulum; Na+/Ca2+ exchange


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