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Depolarization-induced movement of Mn 2 cations across the cell membrane in the guinea pig myocardium
Abstract:
The effects of Mn-2+-containing solutions on the mechanical and electrical responses of myocardial tissue were studied on guinea pig ventricular strips. At a concentration of 10 mM, Mn-2+ abolished the twitch responses and caused the development of a contracture in stimulated preparations but not in resting or in Ca-2+-depleted preparations. The duration of action potentials was shortened, and dV/dt-max was decreased. In Ca-2+-depleted (0.1 mM), Mg-2+-free medium, Mn-2+ also increased the amplitude of the overshoot; the increase was due to a slow phase of depolarization. Measurement of the Mn-2+ uptake showed an increased influx of these ions in stimulated preparations compared with that in quiescent preparations. These results suggest that Mn-2+ (1) generates a transmembrane current in guinea pig myocardial cells and (2) interferes with the excitation-contraction coupling process at two levels: the cell membrane and an intracellular site.
Insights
Manganese (Mn-2+) ions abolish twitch responses and cause contracture in guinea pig heart tissue by affecting electrical activity and excitation-contraction coupling. This study reveals Mn-2+ impacts both cell membrane and intracellular processes.
Area of Science:
- Cardiovascular Physiology
- Cellular Electrophysiology
- Trace Metal Toxicology
Background:
- Myocardial tissue function relies on precise ionic balance for electrical and mechanical activity.
- Manganese (Mn-2+) is a divalent cation with known biological effects, but its specific impact on cardiac contractility and electrophysiology requires detailed investigation.
- Understanding ion channel modulation is crucial for comprehending cardiac arrhythmogenesis and contractility disorders.
Purpose of the Study:
- To investigate the effects of manganese (Mn-2+) on the mechanical and electrical properties of guinea pig ventricular myocardial tissue.
- To elucidate the mechanisms by which Mn-2+ influences cardiac excitation-contraction coupling.
- To determine the cellular sites of Mn-2+ action within myocardial cells.
Main Methods:
- Experiments were conducted on isolated guinea pig ventricular myocardial strips.
- Solutions containing specific concentrations of manganese (Mn-2+) were applied to assess mechanical responses (twitch, contracture) and electrical activity (action potential duration, dV/dt-max).
- Manganese (Mn-2+) uptake was measured in stimulated versus quiescent preparations, and experiments were performed in calcium (Ca-2+)-depleted and magnesium (Mg-2+)-free media.
Main Results:
- A concentration of 10 mM Mn-2+ abolished twitch responses and induced contracture in stimulated myocardial preparations.
- Mn-2+ shortened action potential duration and decreased the maximum rate of depolarization (dV/dt-max).
- In Ca-2+-depleted conditions, Mn-2+ increased action potential overshoot amplitude via a slow depolarization phase, and Mn-2+ uptake was higher in stimulated tissues.
Conclusions:
- Manganese (Mn-2+) ions generate a transmembrane current in guinea pig myocardial cells.
- Mn-2+ interferes with excitation-contraction coupling at both the cell membrane and intracellular levels.
- These findings highlight the significant electrophysiological and mechanical effects of Mn-2+ on cardiac tissue, suggesting potential for arrhythmogenesis and contractility dysfunction.