Résumé
The defects identified in the mechanical activity of the hearts from type 1 diabetic animals include alteration of [Ca.sup.2+] signaling via changes in critical processes that regulate intracellular [Ca.sup.2+] concentration. These defects result partially from a dysfunction of cardiac ryanodine receptor calcium release channel (RyR2). The present study was designed to determine whether the properties of the [Ca.sup.2+] sparks might provide insight into the role of RyR2 in the altered [Ca.sup.2+] signaling in cardiomyocytes from diabetic animals when they were analyzed together with [Ca.sup.2+] transients. Basal [Ca.sup.2+] level as well as [Ca.sup.2+]-spark frequency of cardiomyoctes isolated from 5-week streptozotocin (STZ)-induced diabetic rats significantly increased with respect to aged-matched control rats. [Ca.sup.2+] transients exhibited significantly reduced amplitude and prolonged time courses as well as depressed [Ca.sup.2+] loading of sarcoplasmic reticulum in diabetic rats. Spatio-temporal properties of the [Ca.sup.2+] sparks in cardiomyocytes isolated from diabetic rats were also significantly altered to being almost parallel to the changes of [Ca.sup.2+] transients. In addition, RyR2 from diabetic rat hearts were hyperphosphorylated and protein levels of both RyR2 and FKBP12.6 depleted. These data show that STZ-induced diabetic rat hearts exhibit altered local [Ca.sup.2+] signaling with increased basal [Ca.sup.2+] level. Diabetes 54:3082-2088, 2005