Elevated intracellular ca2+ and myofibrillar ca2+ sensitivity cause
iodoacetate-induced muscle contractures.
Ruff, Robert L.
Department of Neurology, Cleveland Veterans Administration Medical
Center and Case Western Reserve University Medical School, Cleveland,
Ohio
APStracts 3:0154R, 1996.
Ischemic stimulation of iodoacetic acid (IAA)-treated rat extensor
digitorum longus (EDL) muscles produced contractures. Similar
ischemic stimulation of control EDL muscles did not result in
contracture. At the onset of contracture: [ATP] was not reduced,
[phosphocreatine?(PCr)] was reduced >75%, [ADP] was increased 9
-fold, [Ca2+] was increased about 11-fold and [inorganic phosphate (P
-i)] increased less in IAA-treated muscles than in stimulated control
muscles. To test whether contracture resulted from elevated [Ca2+],
increased calcium sensitivity of the contractile proteins or both,
this laboratory made skinned fiber activating solutions that
simulated four different conditions: unstimulated IAA-treated and
control muscles, IAA-treated muscles at contracture and ischemically
stimulated control muscles. Skinned EDL fibers had lower single fiber
tensions and reduced calcium sensitivities in activating solutions
that mimicked the conditions in stimulated control muscles compared
with activating solutions that simulated the conditions in
unstimulated muscles. In contrast, the maximum tension was maintained
and calcium sensitivity was increased in activating solutions that
simulated contracture. Tension at contracture resulted from increased
intracellular [Ca2+] and increased myofibrillar Ca2+ sensitivity
compared with the Ca2+ sensitivity of stimulated control fibers.
Received 28 November 1995; accepted in final form 12 April 1996.
APS Manuscript Number R1228-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 1 May 96