Fig. 2.

Mechanisms of contraction in ASM. Many regulatory mechanisms in ASM to control the contraction and relaxation are well recognized. The ectoenzyme CD38 could produce the second messenger cyclic ADP ribose (cADPR), which causes Ca²⁺ release through ryanodine receptor (RyR) channels from sarcoplasmic reticulum (SR). The G-protein coupled receptor (GPCR)-based pathway activates phospholipase C (PLC) and breaks up phosphatidyl diphosphate inositol 2 (PIP₂) into inositol trisphosphate (IP₃) and diacylglycerol (DAG). Intracellular Ca²⁺ binds to intracellular calmodulin (CAM) to alter the phosphorylation status of myosin light chain (MLC) and regulates ASM function. Depletion of Ca²⁺ in SR calcium stores induces Ca²⁺ influx through store-operated Ca²⁺ channel (SOCC). There are other mechanisms that take part in regulating the intracellular ion concentration of ASM and finally affect the contraction and relaxation of them