Bradykinin | EPFL Graph Search

Are you an EPFL student looking for a semester project?

Work with us on data science and visualisation projects, and deploy your project as an app on top of GraphSearch.

Bradykinin (BK) (Greek brady-, slow; -kinin, kīn(eîn) to move) is a peptide that promotes inflammation. It causes arterioles 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 amino acids, and is a physiologically and pharmacologically active peptide of the kinin group of proteins. 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 FDA approved for the treatment of hypertension and heart failure. Bradykinin, sometimes referred to as BK, is a 9–amino acid peptide chain. The amino acid sequence of bradykinin is: Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg (RPPGFSPFR). Its empirical formula is therefore C50H73N15O11. The kinin–kallikrein system makes bradykinin by proteolytic cleavage of its kininogen precursor, high-molecular-weight kininogen (HMWK or HK), by the enzyme kallikrein. Moreover, there is compelling evidence that plasmin, a fibrinolytic enzyme, is able to generate bradykinin after HMWK cleavage. In humans, bradykinin is broken down by many different kininases: 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. Bradykinin is a potent endothelium-dependent vasodilator and mild diuretic, which may cause a lowering of the blood pressure. It also causes contraction of non-vascular smooth muscle in the bronchus and gut, increases vascular permeability and is also involved in the mechanism of pain. During inflammation, it is released locally from mast cells and basophils during tissue damage.

About this result

This page is automatically generated and may contain information that is not correct, complete, up-to-date, or relevant to your search query. The same applies to every other page on this website. Please make sure to verify the information with EPFL's official sources.

Related publications (3)

Gas-phase probes of kinetically trapped peptides

Liudmila Voronina

Gas-phase techniques are promising for studying intrinsically disordered peptides and proteins, as they can be implemented in a conformer-selective way. One of the issues that prevent them from findin

EPFL2016

Conformations of prolyl-peptide bonds in the bradykinin 1-5 fragment in solution and in the gas phase

Thomas Rizzo, Michael Zachary Kamrath, Antoine Louis Claude Masson, Liudmila Voronina, Carsten Baldauf

The dynamic nature of intrinsically disordered peptides makes them a challenge to characterize by solution-phase techniques. In order to gain insight into the relation between the disordered state and

Amer Chemical Soc2016

Spectroscopic studies of kinetically trapped conformations in the gas phase: the case of triply protonated bradykinin

Thomas Rizzo, Liudmila Voronina

Understanding the relation between the gas-phase structure of biological molecules and their solution-phase structure is important when attempting to use gas-phase techniques to address biologically r

Royal Soc Chemistry2015

Related people (1)

Liudmila Voronina

Related concepts (16)

Complement system

The complement system, also known as complement cascade, is a part of the immune system that enhances (complements) the ability of antibodies and phagocytic cells to clear microbes and damaged cells from an organism, promote inflammation, and attack the pathogen's cell membrane. It is part of the innate immune system, which is not adaptable and does not change during an individual's lifetime. The complement system can, however, be recruited and brought into action by antibodies generated by the adaptive immune system.

Angiotensin II receptor blocker

Angiotensin II receptor blockers (ARBs), formally angiotensin II receptor type 1 (AT1) antagonists, also known as angiotensin receptor blockers, angiotensin II receptor antagonists, or AT1 receptor antagonists, are a group of pharmaceuticals that bind to and inhibit the angiotensin II receptor type 1 (AT1) and thereby block the arteriolar contraction and sodium retention effects of renin–angiotensin system. Their main uses are in the treatment of hypertension (high blood pressure), diabetic nephropathy (kidney damage due to diabetes) and congestive heart failure.

Bradykinin

Related courses (1)

BIO-321: Morphology II

Ce cours permet aux étudiants ayant suivi Morphologie I de réviser et d'approfondir leurs connaissances par l'étude de l'anatomie radiologique et du développement. L'origine de malformations fréquente

Related lectures (4)

Bradykinin: Humoral Vasomotricity BIO-321: Morphology II

Explores the discovery and significance of bradykinin in arterial vasomotricity and vasodilation.

Pharmacodynamics and Drug Targets BIO-478: Pharmacology and pharmacokinetics

Explores pharmacodynamics, drug targets, the renin-angiotensin system, ACE inhibitors, diuretics, and exam questions.

Drug Targets: Receptors, Enzymes, and Therapeutics BIO-478: Pharmacology and pharmacokinetics

Explores drug targets, including receptors, enzymes, and therapeutics, covering pharmacodynamics, case studies on NSAIDs, diabetes, and drug toxicity.