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Bradykinin Sale

(Synonyms: 缓激肽) 目录号 : GC35548

An endogenous vasodilator

Bradykinin Chemical Structure

Cas No.:58-82-2

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实验参考方法

Cell experiment:

SW480 cells are pretreated with different concentrations of bradykinin (0, 0.1, 0.5, 1 μM), and then subjected to invasion and migration assays[2].

Animal experiment:

Rats: Bradykinin acetate is applied topically to the surface of the ovary with a thin piece of cotton (7×7 mm square) soaked with the solution. After application for 30 s, the cotton is removed. Each of the stimuli is delivered to the animal after observing stabilization of heart rate and mean arterial pressure[4]. Mouse: Mice are randomly divided into 3 groups: Sham, Model and Bradykinin. Before surgical procedure, the mice of bradykinin group are intraperitoneally injected with bradykinin (10 mg/kg/d) once a day for three days. After ligation, the mice receive bradykinin injection for another two days and analgesic therapy is performed using buprenorphine at 0.1 mg/kg body weight for 3 days. The mice in other groups receive equal saline as control[3].

References:

[1]. Hornig B, et al. Role of bradykinin in mediating vascular effects of angiotensin-converting enzyme inhibitors inhumans. Circulation. 1997 Mar 4;95(5):1115-8.
[2]. Wang G, et al. Bradykinin stimulates IL-6 production and cell invasion in colorectal cancer cells. Oncol Rep. 2014 Oct;32(4):1709-14.
[3]. Dong R, et al. Exogenous Bradykinin Inhibits Tissue Factor Induction and Deep Vein Thrombosis via Activating the eNOS/Phosphoinositide 3-Kinase/Akt Signaling Pathway. Cell Physiol Biochem. 2015;37(4):1592-606.
[4]. Uchida S, et al. Afferent fibers involved in the bradykinin-induced cardiovascular reflexes from the ovary in rats. Auton Neurosci. 2015 Dec;193:57-62.
[5]. Liu LT, et al. Effect of vascular bradykinin on pancreatic microcirculation and hemorheology in rats with severe acute pancreatitis. Eur Rev Med Pharmacol Sci. 2015;19(14):2646-50.

产品描述

Bradykinin is an endogenous vasodilator that is also involved in inflammation.1,2 It is formed from kininogen via cleavage of high molecular weight kininogen (HMWK) by kallikrein or prekallikrein in a Factor XIIa-dependent or -independent manner.3 Bradykinin binds to the bradykinin B2 receptor (IC50 = 0.54 nM in COS-7 cells expressing the human receptor) and acts as an agonist but does not bind the bradykinin B1 receptor (Ki = >10,000 nM in HEK293 cells expressing the human receptor).4,5 It stimulates arachidonic acid release in CHO cells expressing the human bradykinin B2 receptor (EC50 = 0.7 nM).4 Bradykinin (100 nM) induces relaxation of isolated porcine coronary arterial rings precontracted with acetylcholine or phorbol 12,13-dibutyrate .1 It induces hyperalgesia in mice when administered at a dose of 1 ?g/paw, an effect that can be reversed by the bradykinin B2 antagonist icatibant .2 Plasma levels of bradykinin are increased in patients during an acute attack of angioedema.6

1.Weintraub, N.L., Fang, X., Kaduce, T.L., et al.Potentiation of endothelium-dependent relaxation by epoxyeicosatrienoic acidsCirc. Res.81258-267(1997) 2.Ferreira, S.H., Lorenzetti, B.B., and Poole, S.Bradykinin initiates cytokine-mediated inflammatory hyperalgesiaBr. J. Pharmacol.110(3)1227-1231(1993) 3.Joseph, K., Tholanikunnel, B.G., and Kaplan, A.P.Factor XII-independent cleavage of high-molecular-weight kininogen by prekallikrein and inhibition by C1 inhibitorJ. Allergy Clin. Immunol.124(1)143-149(2009) 4.Hess, J.F., Borkowski, J.A., Macneil, T., et al.Differential pharmacology of cloned human and mouse B2 bradykinin receptorsMol. Pharmacol.45(1)1-8(1994) 5.Bastian, S., Loillier, B., Paquet, J.L., et al.Stable expression of human kinin B1 receptor in 293 cells: Pharmacological and functional characterizationBr. J. Pharmacol.122(2)393-399(1997) 6.Nussberger, J., Cugno, M., Amstutz, C., et al.Plasma bradykinin in angio-oedemaLancet351(9117)1693-1697(1998)

Chemical Properties

Cas No. 58-82-2 SDF
别名 缓激肽
分子式 C50H73N15O11 分子量 1060.21
溶解度 Water: ≥ 100 mg/mL (94.32 mM) 储存条件 Store at -20°C
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1 mM 0.9432 mL 4.716 mL 9.4321 mL
5 mM 0.1886 mL 0.9432 mL 1.8864 mL
10 mM 0.0943 mL 0.4716 mL 0.9432 mL
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Research Update

Bradykinin receptor antagonists

Med Res Rev 1990 Apr-Jun;10(2):237-69.PMID:2158607DOI:10.1002/med.2610100204.

Bradykinin and its active metabolites are produced at the sites of their actions by kallikreins. They potently elicit a variety of biological effects: hypotension, bronchoconstriction, gut and uterine contraction, epithelial secretion in airway, gut, and exocrine glands, vascular permeability, pain, connective tissue proliferation, and eicosanoid formation. These effects are mediated by at least two broad classes of receptors. The most common is the B2 subtype. The Stewart and Vavrek peptides characterized by a DPhe7 substitution have provided powerful tools for study of Bradykinin's actions by competitively and specifically blocking Bradykinin B2 receptors. The significance of kinins in certain human diseases is being explored using these new tools and potential therapeutic agents. At present, human clinical trials are underway to test the usefulness of Bradykinin receptor antagonists in the symptoms of the common cold and in the pain associated with severe burns. Trials for use in asthma will be initiated in 1990.

Bradykinin antagonists: discovery and development

Peptides 2004 Mar;25(3):527-32.PMID:15134872DOI:10.1016/j.peptides.2003.10.016.

Practical Bradykinin antagonists were discovered in 1984 by Vavrek and Stewart and reported in "Peptides." At that time there was already much evidence for involvement of Bradykinin in inflammation and pain, so the specific, competitive antagonists were widely accepted and applied. The key to conversion of Bradykinin into an antagonist was replacement of the proline residue at position 7 with a D-aromatic amino acid. Other modifications converted the initial weak antagonists into modern peptides which are totally resistant to all degrading enzymes, are orally available, and have been used in clinical trials. Non-peptide Bradykinin antagonists have also been developed.

Bradykinin antagonists as anti-cancer agents

Curr Pharm Des 2003;9(25):2036-42.PMID:14529414DOI:10.2174/1381612033454171.

The nonapeptide Bradykinin is an important growth factor for many cancers. Certain peptide and non-peptide Bradykinin antagonists show remarkable anti-cancer activities in both in vitro and in vivo cancer models, especially of lung and prostate cancers. Bradykinin antagonists stimulate apoptosis in cancers by a novel "biased agonist" mechanism: they block intracellular increase of calcium concentration but stimulate the MAP kinase pathway. This unbalanced effect stimulates caspase activation. In nude mouse xenotransplants of lung and prostate cancers the antagonists inhibit angiogenesis and activation of membrane metalloproteases (MMP 2 and 9). In the xenotransplants certain Bradykinin antagonists showed higher potency than standard anti-cancer drugs, without evident toxicity to the hosts. These compounds offer great promise for development of new anti-cancer drugs.

Bradykinin antagonists: development and applications

Biopolymers 1995;37(2):143-55.PMID:7893946DOI:10.1002/bip.360370208.

Bradykinin (BK) is involved in regulation of every major physiological system and is an initiator or mediator of many pathophysiological conditions. Rapid progress in understanding these aspects of BK biology has come since the discovery of BK antagonists. This article reviews principal points in the history of the kallikrein-kinin field and of kinin biology. The chemistry and development of antagonists for B1 and B2 kinin receptors is discussed. Uses of the antagonists in biomedical research and potential clinical applications are presented.

Bradykinin as an endogenous myocardial protective substance with particular reference to ischemic preconditioning--a brief review of the evidence

Can J Physiol Pharmacol 1995 Jul;73(7):837-42.PMID:8846418DOI:10.1139/y95-114.

The present brief review summarizes the evidence for the possibility that endogenously released Bradykinin plays a major role in protecting the heart against the consequences of acute myocardial injury. This evidence includes the facts that kinins are generated under myocardial ischemia; that when they are administered, they are cardioprotective (e.g., antiarrhythmic); that drugs that enhance the release of Bradykinin from the ischemic heart reduce the ischemic injury and, conversely, drugs that block Bradykinin receptors attenuate the reduction in ischemic injury resulting from the release of, or administration of, Bradykinin. The possible mechanism of Bradykinin in the cardioprotection afforded by ischemic preconditioning is summarized. Ischemic preconditioning can be defined as the marked reduction in the severity of ischemic changes that result from coronary artery occlusion when that occlusion is preceded by brief periods of myocardial ischemia, either regional or global, induced, for example, by complete or partial coronary artery occlusion or by rapid ventricular pacing. The possible mechanisms of cardioprotection elicited by Bradykinin (and ischemic preconditioning) are summarized. The most likely is the generation of cyclic GMP within the ischemic myocardium following bradykinin-stimulated nitric oxide generation and release from endothelial cells.