Abstract |
The effects of 50 microM LCB29 ( idrocilamide) were tested on depolarization-induced and caffeine contractures of rat soleus muscle fibers. When applied intracellularly by free diffusion in cut-end voltage-clamped fibers, LCB29 decreased tension amplitude by about 25%. The same amount of inhibition by LCB29 was observed on contractures induced by 6 mM caffeine. The drug did not affect the repriming of caffeine contractures, indicating that internal recycling of calcium was not affected. The voltage-dependent inactivation of tension was facilitated by external application of LCB29. This effect was calcium dependent, so that the greater the external calcium concentration, the greater the drug effectiveness. The spontaneous relaxation of K+ contractures was also accelerated by LCB29. It is concluded that LCB29 acts intracellularly by decreasing sarcoplasmic reticulum calcium release and externally by facilitating the voltage-dependent inactivation of the voltage sensor for excitation-contraction coupling.
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Authors | A Mouzou, A Bouron, J Guillemain, D Guerrier, G Raymond |
Journal | Canadian journal of physiology and pharmacology
(Can J Physiol Pharmacol)
Vol. 71
Issue 12
Pg. 889-95
(Dec 1993)
ISSN: 0008-4212 [Print] Canada |
PMID | 8180884
(Publication Type: Journal Article)
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Chemical References |
- Calcium Channels
- Ethanolamines
- Muscle Relaxants, Central
- Caffeine
- idrocilamide
- Sodium
- Potassium
- Calcium
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Topics |
- Animals
- Caffeine
(pharmacology)
- Calcium
(metabolism, physiology)
- Calcium Channels
(drug effects)
- Depression, Chemical
- Electric Stimulation
- Ethanolamines
(pharmacology)
- Female
- In Vitro Techniques
- Muscle Contraction
(drug effects)
- Muscle Relaxants, Central
(pharmacology)
- Muscle Relaxation
(drug effects)
- Muscles
(cytology, drug effects)
- Potassium
(pharmacology)
- Rats
- Rats, Wistar
- Sarcoplasmic Reticulum
(drug effects, metabolism)
- Sodium
(metabolism, physiology)
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