Am J Physiol Cell Physiol AJP: Heart and Circulatory Physiology
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Am J Physiol Cell Physiol 261: C828-C836, 1991;
0363-6143/91 $5.00
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AJP - Cell Physiology, Vol 261, Issue 5 C828-C836, Copyright © 1991 by American Physiological Society

ARTICLES

Iodoacetate-induced contracture in rat skeletal muscle: possible role of ADP

R. L. Ruff and J. Weissman
Department of Neurology, Cleveland Veterans Affairs Medical Center, Ohio 44106.

The effects of iodoacetic acid (IAA) and ischemic contraction were studied in rat extensor digitorum longus muscles. Ischemic contraction of IAA-treated muscles produced contracture. The onset of contracture was not associated with a change in sarcolemmal electrical properties or reduction in intracellular [ATP]; however, [creatine phosphate] was reduced by 75% and free [ADP] was increased by 665%. Continued stimulation of IAA-treated fibers resulted in depolarization, loss of membrane excitability, further depletion of creatine phosphate, and reduction in [ATP]. The effects seen in IAA-treated muscle did not appear to result from a direct action of IAA on the surface membrane, contractile proteins, or excitation-contraction coupling. The contractures in IAA-treated muscle may have resulted from increased Ca sensitivity of the contractile proteins, increased myoplasmic [Ca], or both. Both effects may have resulted from increased [ADP]. In addition, the reduced acidification during ischemic contraction of IAA-treated fibers compared with control fibers may have further increased the Ca sensitivity of IAA-treated fibers compared with controls.


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R. L. Ruff
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Neurology, October 22, 1999; 53(7): 1556 - 1556.
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