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

Abstract

Abstract Aims/Introduction Abnormalities in Ca2+ 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 Ca2+ 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 Ca2+ channel (LTCC) and Na+/Ca2+ exchanger currents. Fluorescence photometry techniques were used to measure intracellular free Ca2+ concentration. Results Although the LTCC current was not significantly altered, the amplitude of Ca2+ transients increased significantly in EPI‐STZ and ENDO‐STZ compared with controls. Time to peak LTCC current, time to peak Ca2+ transient, time to half decay of LTCC current and time to half decay of Ca2+ transients were not significantly changed in EPI‐STZ and ENDO‐STZ myocytes compared with controls. The Na+/Ca2+ 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 Ca2+ 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+/Ca2+ exchanger. Additional studies are warranted to improve our understanding of the regional impact of diabetes on Ca2+ signaling, which will facilitate the discovery of new targeted treatments for diabetic cardiomyopathy.

Keywords

• Ca2+ transients
• Na+/Ca2+ exchanger
• Streptozotocin‐induced diabetes