Decrease in sodium–calcium exchange and calcium currents in diabetic rat ventricular myocytes

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Abstract
This study was designed in order to gain insight into possible changes in the inward sodium–calcium exchange current (INa–Ca) and theL‐type calcium current (ICa), in ventricular myocytes isolated from streptozotocin‐induced diabetic rats. Recordings were made using the nystatin‐perforated patch technique which minimizes interference with the normal intracellular Ca2+buffering mechanisms. The averagedINa–Cacurrent density elicited by Ca2+current was smaller in diabetic than in normal myocytes at all potentials tested.INa–Caactivated by rapid application of caffeine was significantly reduced and the decay phase was prolonged. The density ofICawas also significantly reduced by diabetes in the range of test potentials between –10 and +50 mV. In addition, the fast time constant ofICainactivation, which represents mainly the sarcoplasmic reticulum (SR) Ca2+release‐induced inactivation, was significantly higher in diabetic than in normal myocytes. The decrease inICa, which is the main source of trigger Ca2+for SR Ca2+release, may explain the significantly lowered peak systolic [Ca2+]ipreviously shown in diabetic myocytes. As activation ofICais essential for subsequent stimulation ofINa–Ca, reducedICamay contribute to decreasing activation of the Na+–Ca2+exchanger.

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