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      The cellular basis of the length-tension relation in cardiac muscle.

      Journal of Molecular and Cellular Cardiology
      Actin Cytoskeleton, ultrastructure, Action Potentials, Animals, Calcium, physiology, Heart, Humans, Myocardial Contraction, Myocardium

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          Abstract

          The relation between muscle length or sarcomere length and developed tension for lengths up to the optimal for contraction (Lmax) is much steeper in cardiac muscle than in skeletal muscle. The steepness of the cardiac length--tension relation arises because the degree of activation of the cardiac myofibrils by calcium increases as muscle length is increased. Two processes contribute to this length-dependence of activation: (i) the calcium sensitivity of the myofibrils increases with muscle length and (ii) the amount of calcium supplied to the myofibrils during systole increases with muscle length. Of these two, the change in calcium sensitivity is the most clearly defined and is responsible for a large part of the rapid change in developed tension when muscle length is altered. It is likely that this change in calcium sensitivity is due to a change in the affinity of troponin for calcium but the underlying mechanism has not been identified. There is good evidence that changes in the calcium supply to the myofibrils can account for the slow changes in tension that follow an alteration in length; there may also be rapid changes in calcium supply but this is less clearly established at present.

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          Journal
          3900426
          10.1016/S0022-2828(85)80097-3

          Actin Cytoskeleton,ultrastructure,Action Potentials,Animals,Calcium,physiology,Heart,Humans,Myocardial Contraction,Myocardium

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