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Bradykinin (BK) (from Greek brady- 'slow' + -kinin, kīn(eîn) 'to move') is a peptide that promotes inflammation. It causes to dilate (enlarge) via the release of prostacyclin, nitric oxide, and endothelium-derived hyperpolarizing factor and makes veins constrict, via prostaglandin F2, thereby leading to leakage into capillary beds, due to the increased pressure in the capillaries. Bradykinin consists of nine , and is a physiologically and pharmacologically active peptide of the kinin group of .
A class of drugs called angiotensin-converting-enzyme inhibitors (ACE inhibitors) increase bradykinin levels by inhibiting its degradation, thereby increasing its blood pressure lowering effect. ACE inhibitors are used to treat hypertension and heart failure.
In humans, bradykinin is broken down by many different -ase: angiotensin-converting enzyme (ACE, kininase II), neprilysin, NEP2, aminopeptidase P (APP), carboxypeptidase N (CPN, kininase I), Carboxypeptidase M, Neutral endopeptidase 24.15, Endothelin converting enzyme-1, Endothelin converting enzyme-2.
During inflammation, it is released locally from and during tissue damage. Specifically in relation to pain, bradykinin has been shown to sensitize TRPV1 receptors, thus lowering the temperature threshold at which they activate, thus presumably contributing to allodynia.
Initial secretion of bradykinin post-natally causes constriction and eventual atrophy of the ductus arteriosus, forming the ligamentum arteriosum between the pulmonary trunk and aortic arch. It also plays a role in the constriction and eventual occlusion of a number of other fetal vessels, including the umbilical arteries and vein. The differential vasoconstriction of these fetal vessels compared to the vasodilator response of other vessels suggests that the walls of these fetal vessels are different from other vessels. (2025). 9780702052309, Elsevier. ISBN 9780702052309
The kinin B1 and B2 receptors belong to G protein coupled receptor (GPCR) family.
In severe cases, the elevation of bradykinin may result in angioedema, a medical emergency. People of African descent have up to five times increased risk of ACE inhibitor induced angioedema due to hereditary predisposing risk factors such as hereditary angioedema. This refractory cough is a common cause for stopping ACE inhibitor therapy.
Overactivation of bradykinin is thought to play a role in a rare disease called hereditary angioedema.
Low levels of bradykinin in the body correlate to with obesity in adolescents; it has been proposed that bradykinin can be used as a biomarker for metabolic syndrome.
Bradykinins have been implicated in a number of cancer progression processes. Increased levels of bradykinins resulting from ACE inhibitor use have been associated with increased lung cancer risks. Bradykinins have been implicated in cell proliferation and migration in gastric cancers, and bradykinin antagonists have been investigated as anti-cancer agents.
Bradykinin has been proposed as an explanation for many symptoms associated with COVID-19, including dry coughs, myalgia, fatigue, nausea, vomiting, diarrhea, anorexia, headaches, decreased cognitive function, arrhythmia, and sudden cardiac death.
Currently, bradykinin inhibitors (antagonists) are being developed as potential therapies for hereditary angioedema. Icatibant is one such inhibitor. Additional bradykinin inhibitors exist. It has long been known in animal studies that bromelain, a substance obtained from the stems and leaves of the pineapple plant, suppresses trauma-induced swelling caused by the release of bradykinin into the bloodstream and tissues. Other substances that act as bradykinin inhibitors include aloe and , substances found in red wine and green tea.
The discovery of bradykinin has led to a new understanding of many physiological and pathological phenomena including circulatory shock induced by venoms and toxins.
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