A general second messenger system mechanism can be broken down into four steps. First, the agonist activates a membrane-bound receptor. Second, the activated G-protein produces a primary effector. Third, the primary effect stimulates the second messenger synthesis. Fourth, the second messenger activates a certain cellular process.
The G-protein coupled receptors for the PIP messenger system produces two effectors, phospholipase C (PLC) and phosphoinositide 3-kinase (PI3K). PLC as an effector produces two different second messengers, inositol triphosphate (IP) and Diacylglycerol (DAG).
IP is soluble and diffuses freely into the cytoplasm. As a second messenger, it is recognized by the inositol triphosphate receptor (IP3R), a Ca channel in the endoplasmic reticulum (ER) membrane, which stores intracellular Ca. The binding of IP to IP3R releases Ca from the ER into the normally Ca-poor cytoplasm, which then triggers various events of Ca signaling. Specifically in blood vessels, the increase in Ca concentration from IP releases nitric oxide, which then diffuses into the smooth muscle tissue and causes relaxation.
DAG remains bound to the membrane by its fatty acid "tails" where it recruits and activates both conventional and novel members of the protein kinase C family. Thus, both IP and DAG contribute to activation of PKCs.
Phosphoinositide 3-kinase (PI3K) as an effector phosphorylates phosphatidylinositol bisphosphate (PIP) to produce phosphatidylinositol (3,4,5)-trisphosphate (PIP). PIP has been shown to activate protein kinase B, increase binding to extracellular proteins and ultimately enhance cell survival.