Key result
Moricizine suppressed the L-type Ca2+ current in a use-dependent manner in guinea-pig ventricular myocytes, potentially explaining action potential shortening by the drug.
Moricizine suppresses the L-type Ca2+ current in a use-dependent manner, providing a possible ionic mechanism for action potential shortening by the drug.
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Hypothesis-generating for moricizine’s Ca2+ effects in animal models; leaves open translation to human electrophysiology.
Whole cell patch clamp techniques were used to study the effects of moricizine on membrane currents in guinea-pig ventricular myocytes. 2. Application of moricizine caused reversible depression of the time-dependent outward K+ current. 3. The Na+/Ca2+ exchange current was not directly affected by moricizine. 4. Although moricizine hardly affected the L-type Ca2+ current when cells were stimulated at a frequency of 0.1 Hz, it suppressed the current at depolarized holding potentials in a use-dependent manner at 1 Hz. 5. Developments of use-dependent block of the Ca2+ current in the presence of moricizine were best expressed by two exponentials. Binding to both activated and inactivated states of the Ca2+ channel were supported from the binding kinetics study. 6. We concluded that moricizine suppressed the L-type Ca2+ current in a use-dependent manner and this might explain, at least in part, action potential shortening by the drug.
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Yamane et al. (1993) studied this question. Moricizine was evaluated on Membrane currents (L-type Ca2+ current, K+ current, Na+/Ca2+ exchange current). Moricizine suppressed the L-type Ca2+ current in a use-dependent manner in guinea-pig ventricular myocytes, potentially explaining action potential shortening by the drug.
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