Calcium is pumped back into sarcoplasmic reticulum by

Depolarization of the T tubule membrane activates the sarcoplasmic reticulum dihydropyridine receptors (DHPR), named for the drug dihydropyridine, which blocks them. DHPR are voltage-gated Ca2+ channels in the T tubule membrane. In cardiac muscle, influx of Ca2+ these channels triggers the release of Ca2+ stored in the sarcoplasmic reticulum (calcium-induced calcium release) by activating the ryanodine receptor (RyR). The RyR is named after the plant alkaloid ryanodine that was used in its discovery. It is a ligand-gated Ca2+ channel with Ca2+ as its natural ligand. In skeletal muscle, Ca2+ entry from the extracellular fluid (ECF) by this route is not required for Ca2+ release. Instead, the DHPR that serves as the voltage sensor unlocks release of Ca2+ from the nearby sarcoplasmic reticulum physical interaction with the RyR. The released Ca2+ is quickly amplified through calcium-induced calcium release. Ca2+ is reduced in the muscle cell by the sarcoplasmic or endoplasmic reticulum Ca2+ ATPase (SERCA) pump. The SERCA pump uses energy from ATP hydrolysis to remove Ca2+ from the cytosol back into the terminal cisterns, where it is stored until released by the next action potential.Ref: Ganong&;s review of medical physiology, 23rd edition, page no:100