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Effect of carnosine on excitation-contraction coupling in mechanically-skinned rat skeletal muscle
This study investigated whether carnosine alters individual processes involved in normal excitation-contraction (E-C) coupling in mammalian skeletal muscle fibres. Mechanically-skinned fibre preparations were utilized because they allow carnosine to be precisely and readily applied to the cytoplasmi...
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Published in: | Journal of muscle research and cell motility 2004-01, Vol.25 (3), p.203-213 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | This study investigated whether carnosine alters individual processes involved in normal excitation-contraction (E-C) coupling in mammalian skeletal muscle fibres. Mechanically-skinned fibre preparations were utilized because they allow carnosine to be precisely and readily applied to the cytoplasmic environment as desired, whilst still retaining the normal E-C coupling mechanism. Carnosine caused an increase (approximately +0.02 to approximately +0.09 pCa units) in Ca2+ -sensitivity of the contractile apparatus in a concentration-dependent manner (i.e. with 4, 8 and 16 mM respectively). Force responses elicited by 8 mM caffeine-induced Ca2+ release from the sarcoplasmic reticulum (SR) were potentiated in the presence of carnosine (compared to the bracketing responses in the absence of carnosine). Force responses elicited by transverse tubular (T-) system depolarization via the dihydropyridine receptors (DHPRs), either by ionic (Na+) substitution or by action potentials (APs), were also potentiated in a concentration-dependent manner in the presence of carnosine. The potentiation of the force responses in all of the various experiments was seemingly totally explicable by the increase in Ca2+-sensitivity of the contractile apparatus caused by carnosine. Thus, these results show that carnosine potentiates force responses solely by 'sensitizing' the contractile apparatus to Ca2+ ions and under physiological conditions does not cause additional Ca2+ release from the SR. |
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ISSN: | 0142-4319 1573-2657 |
DOI: | 10.1023/B:JURE.0000038265.37022.c5 |