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The whole-cell voltage-clamp technique was applied to ventricular myocytes isolated from normal and streptozotocin-induced diabetic rat hearts to investigate the contribution of the calcium current and of the calcium-independent potassium currents to diabetes-induced alterations of the action potential. 2. In single calcium-tolerant isolated myocytes diabetes induced a lengthening of the action potential similar to that previously described in intact ventricular muscles. 3. Only L-type calcium current was present both in normal and diabetic cells. Inactivation of ICa was described in both preparations by two exponentials, whose time constants were not modified by diabetes. 4. Calcium current density-voltage relationships and steady-state inactivation curves were not significantly affected by diabetes. 5. Potassium background inward rectifier current was not modified by diabetes. 6. Calcium-independent outward potassium current inactivated, in both cell types, according to a biexponential process whose time constants were not affected by diabetes. 7. The transient outward potassium current density was significantly reduced by diabetes whereas neither the voltage dependence of the inactivation nor the time dependence of recovery from inactivation was modified. 8. A 4-aminopyridine-insensitive potassium current was also reduced by diabetes. 9. Our results show that in isolated ventricular myocytes the lengthening of the action potential induced by diabetes results mainly from a decrease of the transmembrane calcium-independent potassium permeability.
Jourdon et al. (Fri,) studied this question.