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Nitrendipine blocks high potassium contractures but not twitches in rat skeletal muscle
Abstract:
The effects of the organic calcium channel blocker nitrendipine was tested on electrically evoked twitches and on potassium depolarization-induced contractures of rat lumbricalis muscles. Nitrendipine (10(-7) to 5 X 10(-5) M) blocked only the potassium contractures. It was concluded that blocking calcium uptake through the slow voltage-sensitive calcium channels during potassium depolarization blocks the mechanical response of the muscle. Thus extracellular calcium ions are required for the excitation-contraction (E-C) coupling during depolarization contractures. On the other hand, electrically evoked twitches were not affected by nitrendipine; therefore, extracellular calcium ions entering via the slow voltage-sensitive channels are not required for E-C coupling during the twitch.
Insights
Nitrendipine, a calcium channel blocker, prevented muscle contractions induced by potassium but not electrical stimulation. This indicates extracellular calcium is vital for depolarization-induced contractions, but not for electrically evoked twitches.
Area of Science:
- Pharmacology
- Muscle Physiology
- Cellular Electrophysiology
Background:
- Excitation-contraction (E-C) coupling is crucial for muscle function.
- Voltage-sensitive calcium channels play a role in muscle contraction.
- The specific role of extracellular calcium in different types of muscle activation is not fully elucidated.
Purpose of the Study:
- To investigate the effects of the organic calcium channel blocker nitrendipine on rat lumbricalis muscles.
- To differentiate the role of extracellular calcium in depolarization-induced contractures versus electrically evoked twitches.
Main Methods:
- Rat lumbricalis muscles were subjected to potassium depolarization and electrical stimulation.
- The effects of varying concentrations of nitrendipine (10⁻⁷ to 5 x 10⁻⁵ M) were assessed on muscle mechanical responses.
- Contractile force was measured to quantify the muscle response.
Main Results:
- Nitrendipine selectively blocked potassium depolarization-induced contractures.
- Nitrendipine did not affect electrically evoked twitches.
- The blocking effect on potassium contractures was concentration-dependent.
Conclusions:
- Extracellular calcium influx through slow voltage-sensitive calcium channels is essential for excitation-contraction coupling during potassium depolarization.
- Extracellular calcium influx via slow voltage-sensitive channels is not required for excitation-contraction coupling during electrically evoked twitches.
- Nitrendipine's action highlights distinct calcium signaling pathways in different muscle activation modes.