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Chemical Compound Review:

kallidin1-9 (2S)-2-[[(2S)-1-[(2S)-2- [[(2S)-2-[2-[[(2S)...

Synonyms: kallidin[1-9], CHEMBL264100, CHEBI:412168, DNC005172, AR-1J3381, ...

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Bradykinin, N2-L-lysyl-9-de-L-arginine-

Different from the B(2) agonists, the i.t. injection of DABK or DAKD caused a weak, but prolonged hyperalgesia, an effect that was blocked by the B(1) receptor antagonist des-Arg(9)-[Leu(8)]-bradykinin (DALBK) [1].

High impact information on Bradykinin, N2-L-lysyl-9-de-L-arginine-

We also found that KB-R7943 or 2',4'-dichlorobenzamil, an amiloride analog that inhibits the Na(+)/Ca(2+) exchanger activity, blocked the TGF-beta1- and des-Arg(10)-kallidin-stimulated increases of CTGF mRNA [2].
Activation of the kinin B1 receptor with des-Arg(10)-kallidin stimulated a rise in cytosolic Ca(2+) that was extracellular Na(+)-dependent and extracellular Ca(2+)-dependent [2].
The des-Arg(10)-kallidin-stimulated increase of cytosolic Ca(2+) was blocked by KB-R7943, a specific inhibitor of Ca(2+) entry mode operation of the plasma membrane Na(+)/Ca(2+) exchanger [2].
Because the early signal transduction events regulating CTGF expression are unclear, we investigated the role of Ca(2+) homeostasis in CTGF mRNA expression in TGF-beta1- and des-Arg(10)-kallidin-stimulated human lung myofibroblasts [2].
In addition, B1 receptor activation by des-Arg(10)-kallidin induced a rise in cytosolic Ca(2+) that is consistent with B1 receptor pharmacology [3].

Biological context of Bradykinin, N2-L-lysyl-9-de-L-arginine-

This study examined the up-regulation of haemodynamic and pro-inflammatory responses to the B(1) agonist des-Arg(10)-kallidin (dKD) in a non-human primate model [4].
In addition, B-9870 was a surmontable antagonist of the rabbit B(1)R in the aorta contractility assay, and blocked Lys-des-Arg(9)-BK-induced ERK1/2 phosphorylation in HEK 293 cells expressing a fluorescent B(1)R conjugate [5].
Pretreatment of the neutrophils with the leukotriene B(4) (LTB(4)) antagonist ZK158252 inhibited the LTB(4)-induced chemotaxis as well as the chemotaxis produced by bradykinin and des-Arg(10)-kallidin [6].
We showed that it cleaves the amino-terminal lysyl residue from des-Arg(10)-kallidin to produce des-Arg(9)-bradykinin, suggesting that it plays a role in virulence [7].

Anatomical context of Bradykinin, N2-L-lysyl-9-de-L-arginine-

It antagonized the ¿des-Arg(10)-kallidin-induced contraction of the human umbilical vein (pA(2) = 6.1 +/- 0.1) [8].

Associations of Bradykinin, N2-L-lysyl-9-de-L-arginine- with other chemical compounds

Inhibition of protein synthesis by cycloheximide did not block the des-Arg(10)-kallidin-induced increase in CTGF mRNA [3].

Gene context of Bradykinin, N2-L-lysyl-9-de-L-arginine-

Addition of Lys-des-Arg(9)-BK (1-100 nM) rapidly concentrated the receptor-associated fluorescence into multiple aggregates that remained associated with the plasma membrane (no significant internalization) and colocalized with caveolin-1 [9].
The coexpression of aminopeptidase N and the kinin B(1) receptor in rabbit arterial tissue is of interest for the inactivation of the high-affinity agonist Lys-des-Arg(9)-BK and for the design of hydrosoluble antagonist drugs [10].

References

The use of kinin B1 and B2 receptor knockout mice and selective antagonists to characterize the nociceptive responses caused by kinins at the spinal level. Ferreira, J., Campos, M.M., Araújo, R., Bader, M., Pesquero, J.B., Calixto, J.B. Neuropharmacology (2002) [Pubmed]
Na+/Ca2+ exchanger activity modulates connective tissue growth factor mRNA expression in transforming growth factor beta1- and Des-Arg10-kallidin-stimulated myofibroblasts. Romero, J.R., Rivera, A., Lança, V., Bicho, M.D., Conlin, P.R., Ricupero, D.A. J. Biol. Chem. (2005) [Pubmed]
Des-Arg(10)-kallidin engagement of the B1 receptor stimulates type I collagen synthesis via stabilization of connective tissue growth factor mRNA. Ricupero, D.A., Romero, J.R., Rishikof, D.C., Goldstein, R.H. J. Biol. Chem. (2000) [Pubmed]
Endotoxin sensitization to kinin B(1) receptor agonist in a non-human primate model: haemodynamic and pro-inflammatory effects. deBlois, D., Horlick, R.A. Br. J. Pharmacol. (2001) [Pubmed]
Antagonist, partial agonist and antiproliferative actions of B-9870 (CU201) as a function of the expression and density of the bradykinin B(1) and B(2) receptors. Morissette, G., Houle, S., Gera, L., Stewart, J.M., Marceau, F. Br. J. Pharmacol. (2007) [Pubmed]
Migratory responses of polymorphonuclear leukocytes to kinin peptides. Paegelow, I., Trzeczak, S., Böckmann, S., Vietinghoff, G. Pharmacology (2002) [Pubmed]
A survey for phosphoglucose isomerase with lysyl aminopeptidase activity in Vibrionaceae and non-Vibrio pathogens. Richards, G.P., Parveen, S. Biochim. Biophys. Acta (2005) [Pubmed]
A rational approach to the design and synthesis of a new bradykinin B(1) receptor antagonist. Bedos, P., Amblard, M., Subra, G., Dodey, P., Luccarini, J.M., Paquet, J.L., Pruneau, D., Aumelas, A., Martinez, J. J. Med. Chem. (2000) [Pubmed]
Agonist-induced translocation of the kinin B(1) receptor to caveolae-related rafts. Sabourin, T., Bastien, L., Bachvarov, D.R., Marceau, F. Mol. Pharmacol. (2002) [Pubmed]
Endogenous aminopeptidase N decreases the potency of peptide agonists and antagonists of the kinin B1 receptors in the rabbit aorta. Fortin, J.P., Gera, L., Bouthillier, J., Stewart, J.M., Adam, A., Marceau, F. J. Pharmacol. Exp. Ther. (2005) [Pubmed]

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