Iodoacetate-induced skeletal muscle contracture: changes in ADP, calcium, phosphate, and pH.
The effects of iodoacetic acid (IAA) and ischemic contraction were studied in rat extensor digitorum longus muscles. Ischemic stimulation of IAA-treated muscles produced contracture. We measured total muscle water content, distribution of water between intracellular and extracellular spaces, creatine concentration ([Cr]), creatine phosphate concentration ([PCr]), [ATP], [Pi], intracellular pH, and intracellular Ca2+ concentration ([Ca2+]i) at the onset of contracture. [ADP] was calculated from the equilibrium of the creatine kinase reaction using the measured values of [ATP], [PCr], [Cr], and pH. At the onset of contracture there was a 75% reduction of [PCr], a 12-fold increase in [ADP], and an 11-fold increase in [Ca2+]i compared with unstimulated IAA-treated muscles. [ATP] was not depleted at contracture compared with unstimulated IAA-treated muscles, and [Pi] increased less in muscles at contracture compared with stimulated control muscles. The persistent tension in contractures probably resulted from increased [Ca2+]i combined with increased myofibrillar Ca2+ sensitivity due to elevated [ADP] and relatively reduced intracellular acidification and [Pi].
Ruff
R L
RL
Department of Neurology, Cleveland Veterans Affairs Medical Center, Ohio.
Weissman
J
J
D000244:Adenosine Diphosphate / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000502:physiology*; D004558:Electric Stimulation; D006863:Hydrogen-Ion Concentration; D007425:Intracellular Membranes / Q000378:metabolism; D007461:Iodoacetates / Q000494:pharmacology*; D008297:Male; D008564:Membrane Potentials; D009119:Muscle Contraction / Q000502:physiology*; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D009994:Osmolar Concentration; D010710:Phosphates / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
D007461:Iodoacetates; D010710:Phosphates; D000244:Adenosine Diphosphate; D002118:Calcium