Increasing evidence indicates that hypertension and hypertensive end
organ damage are not only mediated by hemodynamic injury but that
inflammation plays an important role in the pathophysiology and
contributes to the deleterious consequences of this disease. The
complement system is an ancient part of innate immunity comprising
multiple serum proteins and cellular receptors that protect the host
from a hostile microbial environment and maintain tissue and cell
integrity through the elimination of altered or dead cells. As an
important effector arm of innate immunity, it plays also central roles
in the regulation of adaptive immunity. Innate and adaptive immune
responses have been identified as crucial players in the pathogenesis of
arterial hypertension and hypertensive end organ damage. Thus,
complement activation may drive the pathology of hypertension and
hypertensive injury through its impact on innate and adaptive immune
responses aside from direct effects on the vasculature. Indeed, recent
experimental data strongly support a role for complement in all stages
of arterial hypertension and hypertensive end organ damage. The
remarkably similar clinical and histopathological features of malignant
nephrosclerosis and atypical hemolytic uremic syndrome, which is driven
by complement activation, suggest also a role for complement also in the
development of malignant nephrosclerosis. We herein review the role of
complement proteins in hypertension and hypertensive end organ damage.