Resting Ca2+ concentration in the myoplasm is between 10-7 and 10-8 mol/l. The resting state is maintained by the storage of Ca2+ in the sarcoplasmic reticulum where it binds to a specific Ca2+-binding protein called calsequestrin. Calcium ions are released when the sarcolemma is depolarized and the wave of depolarization spreads into the depths of the cell via the T tubules. A calcium release channel in the sarcoplamic reticulum opens and Ca2+ passes from the sarcoplasmic reticulum into the myoplasm; myoplasmic Ca2+ concentrations increase to 10-5 mol/1. The calcium binding sites on troponin C are occupied and muscle contraction takes place by the mechanisms discussed above.
Adm Myelin 1*0
Energised rroEs bndgfl
The Ca2+ release channel is also known as the ryanodine receptor (after a plant alkaloid). It has a transmembraneous part and a section that projects into the myoplasm where it bridges the gap between the sarcoplasmic reticulum and the sarcolemma. It also lies close to the dihydropyridine receptor (a slow Ca2+ channel) of the T tubular system and the two proteins may be coupled.
Relaxation occurs when myoplasmic Ca2+ falls due to re-uptake by the sarcoplasmic reticulum and this is an energy consuming process. Troponin C loses its Ca2+ and the myosin head detaches from the actin filament. Factors that diminish the re-uptake of Ca2+ such as profound fatigue and ischaemia decrease the ability of the muscle to relax and it tends towards the rigidity seen in rigor mortis.
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