The kinin–kallikrein system or simply kinin system is a poorly understood system, not much research has been carried out on this, of blood proteins that play a role in inflammation, blood pressure control, coagulation and pain. Its important mediators bradykinin and kallidin are vasodilators and act on many cell types.
The system was discovered in 1909 (Abelous & Bardier) when researchers discovered that injection with urine (high in kinins) led to hypotension (low blood pressure). The researchers Emil Karl Frey, Heinrich Kraut and Eugen Werle discovered high-molecular weight kininogen in urine around 1930.
Etymology: kinin [Gk] kīn(eîn) to move, set in motion. kallikrein [Gk ] kalli~ sweet and krein = kreos, flesh, named for the pancreatic extracts where it was first discovered
The system consists of a number of large proteins, some small polypeptides and a group of enzymes that activate and deactivate the compounds.
HMWK and LMWK are formed by alternative splicing of the same gene.
Inhibition of ACE with ACE inhibitors leads to decreased conversion of angiotensin I to angiotensin II (a vasoconstrictor) but also to an increase in bradykinin due to decreased degradation. This explains why some patients taking ACE inhibitors develop a dry cough, and some react with angioedema, a dangerous swelling of the head and neck region.
There are hypotheses that many of the ACE-inhibitors' beneficial effects are due to their influence on the kinin-kallikrein system. This includes their effects in arterial hypertension, in ventricular remodeling (after myocardial infarction) and possibly diabetic nephropathy.
Defects of the kinin-kallikrein system in diseases are not generally recognized. The system is the subject of much research due to its relationship to the inflammation and blood pressure systems. It is known that kinins are inflammatory mediators that cause dilation of blood vessels and increased vascular permeability. Kinins are small peptides produced from kininogen by kallikrein and are broken down by kininases. They act on phospholipase and increase arachidonic acid release and thus prostaglandin (PGE2) production.
C1-inhibitor is a serine protease inhibitor (serpin) protein. C1-INH is the most important physiological inhibitor of plasma kallikrein, fXIa and fXIIa. C1-INH also inhibits proteinases of the fibrinolytic, clotting, and kinin pathways. Deficiency of C1-INH permits plasma kallikrein activation, which leads to the production of the vasoactive peptide bradykinin.
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