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Chemical Compound Review

BRADYKININ     (2S)-2-[[(2S)-2-[[(2S)-1- [(2S)-2-[[(2S)-2...

Synonyms: L-Bradykinin, Callidin I, Kallidin 9, Kallidin I, CHEMBL406291, ...
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Disease relevance of BRADYKININ


Psychiatry related information on BRADYKININ

  • The BK response was limited to an initial transient peak with the exception of a few cells, which after a prolonged latency period, exhibited weak but regular base-line oscillations [6].

High impact information on BRADYKININ

  • In this article Amrita Ahluwalia and Mauro Perretti briefly describe the biology of BK and its receptors, and discuss the possible development of B1 receptor antagonists as novel anti-inflammatory agents [7].
  • The increase in blood pressure and the decrease in renal BK, nitric oxide, and cGMP during AT2-receptor blockade suggests that the AT2 receptor mediates counterregulatory vasodilation in Grollman hypertension and prevents a further increase in blood pressure [2].
  • However, only vessels from Dahl-NT showed dilator responses to SP (10 fmol/L to 1 nmol/L) and BKN (100 fmol/L to 10 nmol/L) [8].
  • Stimulation of B1 and B2 kinin receptors on cultured rabbit superior mesenteric artery smooth muscle cells with des-Arg9-bradykinin (DBK) and bradykinin (BK), respectively, results in significantly different patterns of intracellular Ca2+ mobilization [6].
  • In contrast, the effects of neither BK nor PMA on brain microvessel endothelial cell uptake of Lucifer yellow ere altered by indomethacin pretreatment [9].

Chemical compound and disease context of BRADYKININ

  • 6. The marked increase in conversion of AI to AII in hypertensive animals, accompanied by an increased pulmonary degradation of BK in SHR rats, suggests that ACE activity is increased in conscious SHR and SHRSP rats and may participate in the genesis of hypertension in this model of genetic hypertension [10].

Biological context of BRADYKININ

  • BK at 1.2 +/- 0.2 X 10(-6) M decreased the rate of [3H]-HGG hydrolysis by 50% [11].
  • The (-/-) genotype of a frequent insertion/deletion polymorphism of the B(2)R exon 1 was associated with increased contractile efficiency of the B(1)R agonist, Sar-¿D-Phe(8)des-Arg(9)-BK, but had no effect on BK-induced contractility [12].
  • Moreover, BK has been shown to increase phosphorylation of insulin receptor and its cell substrates [4].
  • Intravenous infusion of a BK antagonist, Hoe140 (3 mg/kg/hr), strongly blocked both EB-induced diuresis and natriuresis [13].
  • 4. In cultured RMIC, AngII, ET, BK, ANP and AVP act on their respective receptors to induce various cellular responses, including contraction, prostaglandin synthesis, cell proliferation and/or extracellular matrix synthesis [14].

Anatomical context of BRADYKININ

  • Nanomolar concentrations of BK and PMA also stimulated Lucifer yellow uptake by the brain microvessel endothelial cell by 40 and 95%, respectively [9].
  • In C2C12 myoblasts, isoform-specific knock-down experiments using siRNA showed that activation of bradykinin (BK) receptor led to stimulation of PLC-beta1 and subsequent intracellular Ca(2+) mobilization [15].
  • Degradation of BK by ACE was calculated to be 52% in the rat uterus and 75% in the rabbit perfused ear [16].
  • Vascular rings from 100 different umbilical cords were submitted to a standardized protocol where E(max) values were obtained at 2 and 6 h of incubation, and EC(50) values were estimated at 6 h for the B(1)R agonist Sar-¿D-Phe(8)des-Arg(9)-BK; E(max) and EC(50) values were also obtained for the B(2)R agonist BK at 4 h [12].
  • Luminometry of healthy fibroblasts expressing either aequorin or luciferase in the mitochondrial matrix showed that rhod-2 dose dependently decreased the Bk-induced increase in [Ca2+]M and [ATP]M by maximally 80 and 90%, respectively [17].

Associations of BRADYKININ with other chemical compounds

  • Compounds structurally unrelated to BK, such as 5Q20881, pGlu-Lys-Trp-Ala-Pro-OH (BPP5a) and angiotensin I, inhibited T1K binding and [3H]-HGG hydrolysis by ACE [11].
  • In immunized animals, treated with colchicine (1 mg kg(-1) i.v.), PE responses to the directly acting mediator, bradykinin (BK), were not affected, whereas PE responses to the neutrophil dependent mediator, f-met-leu-phe (fMLP), were significantly (P<0.01) reduced [18].
  • 2. Captopril augmented the BK-induced contractions of the rat isolated uterus, the BK- and substance P-induced contractions of the guinea-pig ileum, and the BK-induced venoconstriction in the isolated perfused ear of the rabbit [16].
  • TNF-alpha (0.00417, 0.0417, 0.417, and 1.25 micrograms/ml) incubated with BPA for 60 min inhibited EDR of the BPA to ACh, BK, and histamine [19].
  • When the dog common carotid artery is desensitized with high concentrations of SP, BK, eledoisin, and physalaemin a cross-desensitization is observed only between SP and physalaemin [20].

Gene context of BRADYKININ


Analytical, diagnostic and therapeutic context of BRADYKININ

  • Patients underwent two treadmill exercise tests and determination of forearm vasodilator response to BK [1].
  • This was prevented by CE inhibition and/or perfusion with bradykinin (BK), which in turn could be competitively antagonized with a BK antagonist [25].
  • Neither hypophysectomy nor inhibition of corticosteroid synthesis affected BK-induced PE in female or male rats [26].
  • Castration in male rats decreased BK-induced PE, and administration of testosterone or its nonmetabolizable analog dihydrotestosterone reconstituted the male phenotype [26].
  • Adrenal denervation in females produced the same magnitude increase in BK-induced PE as adrenalectomy or ovariectomy, suggesting that the adrenal medullary factor(s) in females may account for the female sex steroid effect on BK-induced PE [26].


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  2. Protective role of the angiotensin AT2 receptor in a renal wrap hypertension model. Siragy, H.M., Carey, R.M. Hypertension (1999) [Pubmed]
  3. Characterization of thimet- and neurolysin-like activities in Escherichia coli M 3 A peptidases and description of a specific substrate. Paschoalin, T., Carmona, A.K., Oliveira, V., Juliano, L., Travassos, L.R. Arch. Biochem. Biophys. (2005) [Pubmed]
  4. The kallikrein-kinin system, angiotensin converting enzyme inhibitors and insulin sensitivity. Damas, J., Garbacki, N., Lefèbvre, P.J. Diabetes Metab. Res. Rev. (2004) [Pubmed]
  5. Role of the mediators in pulmonary hyperreactivity: the cocktail interaction hypothesis. Omini, C., Brunelli, G., Hernandez, A., Daffonchio, L. The European respiratory journal. Supplement. (1989) [Pubmed]
  6. B1 and B2 kinin receptors mediate distinct patterns of intracellular Ca2+ signaling in single cultured vascular smooth muscle cells. Mathis, S.A., Criscimagna, N.L., Leeb-Lundberg, L.M. Mol. Pharmacol. (1996) [Pubmed]
  7. B1 receptors as a new inflammatory target. Could this B the 1? Ahluwalia, A., Perretti, M. Trends Pharmacol. Sci. (1999) [Pubmed]
  8. Distinct endothelial impairment in coronary microvessels from hypertensive Dahl rats. Gauthier-Rein, K.M., Rusch, N.J. Hypertension (1998) [Pubmed]
  9. Angiotensin peptide regulation of fluid-phase endocytosis in brain microvessel endothelial cell monolayers. Guillot, F.L., Audus, K.L. J. Cereb. Blood Flow Metab. (1990) [Pubmed]
  10. Angiotensin converting activity assessed in vivo is increased in hereditary hypertensive rats. Krieger, E.M., Yamori, Y., Lovenberg, W.M. Braz. J. Med. Biol. Res. (1992) [Pubmed]
  11. Interactions of kinins with angiotensin I converting enzyme (kininase II). Odya, C.E., Wilgis, F.P., Vavrek, R.J., Stewart, J.M. Biochem. Pharmacol. (1983) [Pubmed]
  12. Effect of allelic polymorphism of the B(1) and B(2) receptor genes on the contractile responses of the human umbilical vein to kinins. Houle, S., Landry, M., Audet, R., Bouthillier, J., Bachvarov, D.R., Marceau, F. J. Pharmacol. Exp. Ther. (2000) [Pubmed]
  13. Diuretic and natriuretic effect of ebelactone B in anesthetized rats by inhibition of a urinary carboxypeptidase Y-like kininase. Majima, M., Kuribayashi, Y., Ikeda, Y., Adachi, K., Kato, H., Katori, M., Aoyagi, T. Jpn. J. Pharmacol. (1994) [Pubmed]
  14. Renomedullary interstitial cells: a target for endocrine and paracrine actions of vasoactive peptides in the renal medulla. Zhuo, J.L. Clin. Exp. Pharmacol. Physiol. (2000) [Pubmed]
  15. Inhibition of phospholipase C-beta1-mediated signaling by O-GlcNAc modification. Kim, Y.H., Song, M., Oh, Y.S., Heo, K., Choi, J.W., Park, J.M., Kim, S.H., Lim, S., Kwon, H.M., Ryu, S.H., Suh, P.G. J. Cell. Physiol. (2006) [Pubmed]
  16. Demonstration of extrapulmonary activity of angiotensin converting enzyme in intact tissue preparations. Lembeck, F., Griesbacher, T., Eckhardt, M. Br. J. Pharmacol. (1990) [Pubmed]
  17. Ca2+-mobilizing agonists increase mitochondrial ATP production to accelerate cytosolic Ca2+ removal: aberrations in human complex I deficiency. Visch, H.J., Koopman, W.J., Zeegers, D., van Emst-de Vries, S.E., van Kuppeveld, F.J., van den Heuvel, L.W., Smeitink, J.A., Willems, P.H. Am. J. Physiol., Cell Physiol. (2006) [Pubmed]
  18. A comparison of allergen and polycation induced cutaneous responses in the rabbit. Jones, H., Paul, W., Page, C.P. Br. J. Pharmacol. (2001) [Pubmed]
  19. Tumor necrosis factor-alpha inhibits endothelium-dependent relaxation. Greenberg, S., Xie, J., Wang, Y., Cai, B., Kolls, J., Nelson, S., Hyman, A., Summer, W.R., Lippton, H. J. Appl. Physiol. (1993) [Pubmed]
  20. The dog common carotid artery: a sensitive bioassay for studying vasodilator effects of substance P and of kinins. Couture, R., Gaudreau, P., St-Pierre, S., Regoli, D. Can. J. Physiol. Pharmacol. (1980) [Pubmed]
  21. G-protein-coupled receptor agonists differentially regulate basal or tumor necrosis factor-alpha-stimulated activation of interleukin-6 and RANTES in human airway smooth muscle cells. Huang, C.D., Ammit, A.J., Tliba, O., Kuo, H.P., Penn, R.B., Panettieri, R.A., Amrani, Y. J. Biomed. Sci. (2005) [Pubmed]
  22. Structural diversity of angiotensin-converting enzyme. Bingham, R.J., Dive, V., Phillips, S.E., Shirras, A.D., Isaac, R.E. FEBS J. (2006) [Pubmed]
  23. Kinins are involved in the antiproteinuric effect of angiotensin-converting enzyme inhibition in experimental diabetic nephropathy. Tschöpe, C., Seidl, U., Reinecke, A., Riester, U., Graf, K., Schultheiss, H.P., Hilgenfeldt, U., Unger, T. Int. Immunopharmacol. (2003) [Pubmed]
  24. Inhibition of both angiotensin-converting enzyme and neutral endopeptidase by S21402 (RB105) in rats with experimental myocardial infarction. Gonzalez, W., Beslot, F., Laboulandine, I., Fournié-Zaluski, M.C., Roques, B.P., Michel, J.B. J. Pharmacol. Exp. Ther. (1996) [Pubmed]
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  26. Sex steroid regulation of the inflammatory response: sympathoadrenal dependence in the female rat. Green, P.G., Dahlqvist, S.R., Isenberg, W.M., Strausbaugh, H.J., Miao, F.J., Levine, J.D. J. Neurosci. (1999) [Pubmed]
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