Fig. 12.8 ) reflects release of Ca++ from the terminal cisternae via the RYR and reuptake primarily into the longitudinal portion of the SR by SERCA. The low-affinity Ca++-binding protein sarcalumenin is present throughout the longitudinal tubules of the SR and nonjunctional regions of the terminal cisternae and is thought to be involved in the transfer of Ca++ from sites of Ca++ uptake in the longitudinal tubules to sites of Ca++ release in the terminal cisternae. Results of studies suggest that sarcalumenin increases Ca++ uptake by SERCA, at least in part by buffering luminal
Ca++ near the pump.
The endogenous micropeptides phospholamban, sarcolipin, and myoregulin have been shown to regulate the activity of SERCA by decreasing the Ca sensitivity of Ca uptake (
Fig. 12.11 ). Protein kinase A–dependent phosphorylation of phospholamban in slow-twitch skeletal muscle has been reported to increase Ca transport in the SR, similar to the effect of phospholamban phosphorylation in the heart. Phospholamban and sarcolipin are present in slow-twitch muscle, whereas myoregulin is present in both fastand slow-twitch muscle.
*During the transport of Ca++ , SERCA exchanges two Ca++ ions for two H+ ions (i.e., H+ is pumped out of the SR).
•Fig. 12.10. Molecular Structure and Relationships Between the Dihydropyridine Receptor (DHPR) in the T Tubule Membrane and the Ryanodine Receptor (RYR) in the Sarcoplasmic Reticulum (SR) Membrane. TriadinisanassociatedSRproteinthatmayparticipateintheinteractionofRYRandDHPR.Calsequestrinisalow-affinityCa++-bindingproteinthathelpsaccumulateCa++ intheterminalcisternae.Seetextfordetails.COOH,carboxylicacid.(FromRossiAE,DirksenRT.Sarcoplasmicreticulum:thedynamiccalciumgovernorofmuscle.Muscle Nerve. 2006;33:715.) movement of the associated tropomyosin molecule toward
Actin-Myosin Interaction: the cleft of the actin filament. This movement of tropo myosin exposes myosin binding sites on the actin filament As noted, contraction of skeletal muscle requires an increase and allows a cross-bridge to form and thereby generate in intracellular [Ca++]. Moreover, the process of contraction tension (see section “
Cross-Bridge Cycling: Sarcomere is regulated by the thin filament. As shown in