Calcium currents in ventricular myocytes of prehypertrophic cardiomyopathic hamsters

Possible changes in Ca²⁺ currents (I(Ca)), which might contribute to Ca²⁺ overload in young (70- to 100-day-old) cardiomyopathic (CM) hamster hearts, were determined in isolated ventricular myocytes with conventional recording and discontinuous single-electrode voltage-clamp techniques. Action potential duration at 90% repolarization (APD₉₀) was significantly longer in CM myocytes compared with normal cells (APD₉₀ = 120.3 ± 4.5 vs. 98.2 ± 5.9 ms, P < 0.01). Input resistance, membrane time constant, and membrane capacitance were similar in normal and CM myocytes. Current-voltage (I-V) relations for peak I(Ca) were depressed in CM cells compared with normal cells; this difference was statistically significant at the peak of the I-V curve. Activation and inactivation relations for I(Ca) and recovery from inactivation were similar in myocytes from normal and CM hearts. These changes occurred in myocytes from young CM animals before development of heart failure. Results indicate that increased Ca²⁺ influx through L-type Ca²⁺ channels does not account for the longer APD in cardiomyopathy and is not involved in the development of Ca²⁺ overload in cardiomyopathy.