<P> A protein found in cardiac muscle, called phospholamban (PLB) has been shown to prevent SERCA from working . It does this by binding to the SERCA and decreasing its attraction (affinity) to calcium, therefore preventing calcium uptake into the SR . Failure to remove Ca from the cytosol, prevents muscle relaxation and therefore means that there is a decrease in muscle contraction too . However, molecules such as adrenaline and noradrenaline, can prevent PLB from inhibiting SERCA . When these hormones bind to a receptor, called a beta 1 adrenoceptor, located on the cell membrane, they produce a series of reactions (known as a cyclic AMP pathway) that produces an enzyme called protein kinase A (PKA). PKA can add a phosphate to PLB (this is known as phosphorylation), preventing it from inhibiting SERCA and allowing for muscle relaxation . </P> <P> Located within the SR is a protein called calsequestrin . This protein can bind to around 50 Ca, which decreases the amount of free Ca within the SR (as more is bound to calsequestrin). Therefore more calcium can be stored (the calsequestrin is said to be a buffer). It is primarily located within the junctional SR / terminal cisternae, in close association with the calcium release channel (described below) </P> <P> Calcium ion release from the SR, occurs in the junctional SR / terminal cisternae through a ryanodine receptor (RyR) and is known as a calcium spark . There are three types of ryanodine receptor, RyR1 (in skeletal muscle), RyR2 (in cardiac muscle) and RyR3 (in the brain). Calcium release through ryanodine receptors in the SR is triggered differently in different muscles . In cardiac and smooth muscle an electrical impulse (action potential) triggers calcium ions to enter the cell through an L - type calcium channel located in the cell membrane (smooth muscle) or T - tubule membrane (cardiac muscle). These calcium ions bind to and activate the RyR, producing a larger increase in intracellular calcium . In skeletal muscle, however, the L - type calcium channel is bound to the RyR . Therefore activation of the L - type calcium channel, via an action potential, activates the RyR directly, causing calcium release (see calcium sparks for more details). Also, caffeine (found in coffee) can bind to and stimulate RyR . Caffeine works by making the RyR more sensitive to either the action potential (skeletal muscle) or calcium (cardiac or smooth muscle) therefore producing calcium sparks more often (this can result in increased heart rate, which is why we feel more awake after coffee). </P> <P> Triadin and Junctin are proteins found within the SR membrane, that are bound to the RyR . The main role of these proteins is to anchor calsequestrin (see above) to the ryanodine receptor . At' normal' (physiological) SR calcium levels, calsequestrin binds to the RyR, Triadin and Junctin, which prevents the RyR from opening . If calcium concentration within the SR falls too low, there will be less calcium bound to the calsequestrin . This means that there is more room on the calsequestrin, to bind to the junctin, triadin and ryanodine receptor, therefore it binds tighter . However, if calcium within the SR rises too high, more calcium binds to the calsequestrin and therefore it binds to the junctin - triadin - RyR complex less tightly . The RyR can therefore open and release calcium into the cell . </P>

What triggers the release of calcium from the sarcoplasmic reticulum
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