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Calcium currents in ventricular myocytes of prehypertrophic cardiomyopathic hamsters
G R Li1, G R Ferrier, S E Howlett
1Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada.
Insights
Calcium overload in young hearts with cardiomyopathy is not caused by increased calcium currents. These findings in cardiomyopathic (CM) hamster hearts reveal normal calcium channel function before heart failure onset.
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Cardiomyopathy (CM) can lead to calcium overload in heart cells.
- Early detection of CM mechanisms is crucial for understanding disease progression.
Purpose of the Study:
- To investigate potential changes in calcium currents (ICa) contributing to calcium overload in young cardiomyopathic (CM) hamster hearts.
- To determine if altered calcium influx through L-type calcium channels is involved in the early stages of cardiomyopathy.
Main Methods:
- Utilized conventional recording and discontinuous single-electrode voltage-clamp techniques.
- Isolated ventricular myocytes from young (70-100 days old) normal and CM hamsters.
- Measured action potential duration (APD90), input resistance, membrane time constant, membrane capacitance, and current-voltage (I-V) relations for peak ICa.
Main Results:
- Action potential duration at 90% repolarization (APD90) was significantly longer in CM myocytes (120.3 ms) compared to normal myocytes (98.2 ms).
- Peak ICa current-voltage (I-V) relations were depressed in CM cells, with significant differences observed.
- No significant differences were found in input resistance, membrane time constant, membrane capacitance, or activation/inactivation properties of ICa between normal and CM myocytes.
Conclusions:
- Increased calcium influx via L-type calcium channels does not explain the prolonged APD in early-stage cardiomyopathy.
- Altered calcium currents are not the primary cause of calcium overload in young CM hearts before the onset of heart failure.
Abstract:
Possible changes in Ca2+ currents (ICa), 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 ICa 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 ICa 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.