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Kinin-kallikrein systemThe kinin-kallikrein system or simply kinin system is a poorly delineated system of blood proteins that plays a role in inflammation, blood pressure control, coagulation and pain. Its important mediators bradykinin and kallidin are vasodilators and act on many cell types. Additional recommended knowledge
HistoryThe system was discovered in 1909 (Abelous & Bardier) when researchers discovered that injection with urine (high in kinins) led to hypotension (low blood pressure).[1] The researchers Emil Karl Frey, Heinrich Kraut and Eugen Werle discovered high-molecular weight kininogen in urine around 1930.[2] MembersThe system consists of a number of large proteins, some small polypeptides and a group of enzymes that activate and deactivate the compounds. ProteinsHigh-molecular weight kininogen (HMWK) and low-molecular weight kininogen (LMWK) are precursors of the polypeptides. They have activity of themselves.
Polypeptides
HMWK and LMWK are formed by alternative splicing of the same gene.[3] Enzymes
PharmacologyInhibition of ACE with ACE inhibitors leads to a decrease in angiotensin (a vasoconstrictor) but also to an increase in bradykinin due to decreased degradation. This explains why some patients of ACEi's 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. Role in diseaseDefects 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. References
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This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Kinin-kallikrein_system". A list of authors is available in Wikipedia. |