The Sarco(Endo)Plasmic Reticulum Ca2+ Pumps in the Cardiovascular System

The sarcoplasmic reticulum (SR) is of major importance in the electrochemical coupling in striated muscle. In the heart, approximately 80% of the Ca2+ used for the contraction-relaxation cycle is released from SR through the Ca2+-induced Ca2+-release mechanism. In smooth muscle, SR is essential in the pharmacochemical coupling. The effect on contraction of many agonists which act through the activation of the phospholipase C cascade and production of inositol 1,4,5-trisphosphate (IP3) is dependent on the release of Ca2+ from internal stores. On the other hand, entry of Ca2+ from the extracellular space induces local increases in Ca2+ concentration sufficient to release Ca2+ from the SR/ER of cardiac and smooth muscle cells by the Ca2+-induced Ca2+-release mechanism activated by the ryanodine receptor (RyR). Calcium plays a role in endothelial cell signaling as a messenger for the release of endothelial factors regulating vascular smooth muscle and cardiac contractility. Both transsarcolemmal Ca2+ flux and release from internal stores are responsible for the agonists-induced increase in cytoplasmic Ca2+ concentration. In endothelial cells, the IP3-induced Ca2+- release is the major mechanism in the Ca2+ signaling pathway but the existence of the Ca2+-induced Ca2+-release mechanism and the presence of ryanodine receptors were also demonstrated [1].