Calcium ion channel pumps ions into Sarcoplasmic Reticulum utilizing active transport as this is against the concentration gradient. Calcium is taken in when ATP along with 2 calcium ions binds to the cytosolic side of the pump.
The hydrolysis of ATP causes structural alterations of the pump. This leads to the opening of the channel through which the calcium ions pass through into the Sarcoplasmic Reticulum.
The calcium ions are released through the activation of RyR receptors at the terminal cisternae. This causes a surge in ion concentration causes calcium spark that can be spontaneous or evoked.
Calcium-induced calcium release is a mechanism for triggering calcium release. An action potential alters the shape of dihydropyridine receptors resulting in the opening of a calcium ion channel.
The resulting influx leads to the binding of calcium ions to RyR. This receptor is activated on binding with 4 calcium ions and this leads to calcium release. This results in the evoked calcium spark and is observed in the case of smooth and cardiac muscles.
In the case of skeletal muscle, RyR receptors open directly when dihydropyridine receptors change and open, and thus, this occurs without prior flooding of calcium ions. Both kinds of receptors are in proximity to each other, such that any change in dihydropyridine receptor shape triggers RyRs.
In cardiac and smooth muscles, the dihydropyridine receptors are not directly in contact with RyR, and hence calcium ion flooding and binding occurs is prerequisite for the release of calcium.
If no sort of action potentials are required for calcium release, then it is termed a spontaneous calcium spark. This mechanism is dependent on the high calcium ion concentration inside the SR.
The RyR opens by either direct binding of calcium ions or the detachment of calsequestrin from the receptor. If the concentration of calcium ions is low, then calsequestrin inhibits the opening of RyR by binding to it.