Altered Ca2+ handling in ventricular myocytes isolated from diabetic rats
| Autor: | K. Le Prigent, K. J. Buckler, Danielle Feuvray, D. Lagadic-Gossmann |
|---|---|
| Rok vydání: | 1996 |
| Předmět: |
Male
medicine.medical_specialty Indoles Heart disease Physiology Heart Ventricles Cardiomyopathy Cell Separation Diabetes Mellitus Experimental Reference Values Physiology (medical) Internal medicine Diabetes mellitus Diabetic cardiomyopathy medicine Myocyte Animals Rats Wistar Fluorescent Dyes Aniline Compounds business.industry Endoplasmic reticulum Myocardium Intracellular Membranes medicine.disease Rats Sarcoplasmic Reticulum Endocrinology Xanthenes Calcium Cardiology and Cardiovascular Medicine business Homeostasis Intracellular |
| Zdroj: | The American journal of physiology. 270(5 Pt 2) |
| ISSN: | 0002-9513 |
| Popis: | It has been suggested that alterations in intracellular Ca2+ homeostasis may be responsible for the development of diabetic cardiomyopathy. We have studied the effects of streptozotocin-induced diabetes on intracellular Ca2+ concentration ([Ca2+]i) in enzymically isolated rat ventricular myocytes. [Ca2+]i was measured using indo 1 or fluo 3. Both diastolic and peak systolic [Ca2+]i were reduced in diabetic compared with normal myocytes (by 52 and 43%, respectively). The decay phase of the systolic [Ca2+]i transient was slower in the diabetic myocyte compared with normal (time constant = 89.6 +/- 3.4 ms, n = 23, normal vs. 105.2 +/- 4.05 ms, n = 20, diabetic; P < 0.01). This led to a significant prolongation of the [Ca2+]i transient duration in the diabetic myocyte. In both normal and diabetic myocytes, increasing the frequency of electrical stimulation decreased peak systolic [Ca2+]i.The relationship between stimulation frequency and normalized peak systolic [Ca2+]i was the same for both normal and diabetic myocytes. We also found that the caffeine-induced Ca2+ release [used as an index of sarcoplasmic reticulum (SR) Ca2+ content] was significantly reduced in diabetic myocytes. These data indicate that SR Ca2+ content is decreased by diabetes. In the presence of thapsigargin (2.5 microM, an inhibitor of SR Ca(2+)-adenosinetriphosphatase), the magnitude and time course of stimulus-evoked [Ca2+]i transients were identical in both groups of myocytes, suggesting that Ca2+ influx and/or efflux across the plasma membrane is not significantly affected in diabetes. We conclude that 1) diabetes is associated with significant alterations in [Ca2+]i homeostasis and 2) the decrease in systolic [Ca2+]i and lengthening of the systolic [Ca2+]i transient result primarily from dysfunction of the SR. |
| Databáze: | OpenAIRE |
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