Figure 1
Complement activation is initiated through three pathways: the classical, alternative or the lectin pathway. Full activation leads to the generation of several biologically active fragments including C5b-9, which ‘seeds’ membrane attack complex (MAC)-mediated direct lysis of pathogens. In addition, complement and extra- as well as intracellular complement receptors also fine shape cells of the innate and the adaptive immune system. Polymorphic neutrophils (PMN) and monocyte/macrophages express anaphylatoxin receptors. Dendritic cells can be identified by expression CD11c, a component of complement receptor 4. Dendritic cells also express the CD11b, a component of complement receptor 3. T cells express anaphylatoxin receptors in different intracellular compartments and on the surface. Intracellular C3 is converted by cathpepsin L to C3a that bind lysosomal C3aR. This drives mammalian target of rapamycin (mTOR) activity that sustains homeostatic cell survival. C5aR1 is found on the surface was well as on mitochondria whereas C5aR2 is only found on the surface. B cells express complement receptors 1 and 2 (CR1/CR2). Complement proteins, innate and adaptive immune cells are potential mediators of hypertension and hypertensive end organ damage. Endothelial dysfunction and injury are most likely the first step of hypertensive end organ injury.