Calcium signaling in endocardial and epicardial ventricular myocytes from streptozotocin‐induced diabetic rats

AIMS/INTRODUCTION: Abnormalities in Ca(2+) signaling have a key role in hemodynamic dysfunction in diabetic heart. The purpose of this study was to explore the effects of streptozotocin (STZ)‐induced diabetes on Ca(2+) signaling in epicardial (EPI) and endocardial (ENDO) cells of the left ventricle after 5–6 months of STZ injection. MATERIALS AND METHODS: Whole‐cell patch clamp was used to measure the L‐type Ca(2+) channel (LTCC) and Na(+)/Ca(2+) exchanger currents. Fluorescence photometry techniques were used to measure intracellular free Ca(2+) concentration. RESULTS: Although the LTCC current was not significantly altered, the amplitude of Ca(2+) transients increased significantly in EPI‐STZ and ENDO‐STZ compared with controls. Time to peak LTCC current, time to peak Ca(2+) transient, time to half decay of LTCC current and time to half decay of Ca(2+) transients were not significantly changed in EPI‐STZ and ENDO‐STZ myocytes compared with controls. The Na(+)/Ca(2+) exchanger current was significantly smaller in EPI‐STZ and in ENDO‐STZ compared with controls. CONCLUSIONS: STZ‐induced diabetes resulted in an increase in amplitude of Ca(2+) transients in EPI and ENDO myocytes that was independent of the LTCC current. Such an effect can be attributed, at least in part, to the dysfunction of the Na(+)/Ca(2+) exchanger. Additional studies are warranted to improve our understanding of the regional impact of diabetes on Ca(2+) signaling, which will facilitate the discovery of new targeted treatments for diabetic cardiomyopathy.