Disease relevance of 1-Des-arg-bradykinin

• Time- and collision energy-resolved surface-induced dissociation (SID) of des-Arg(1)- and des-Arg(9)-bradykinin on a fluorinated self-assembled monolayer (SAM) surface was studied by use of a novel Fourier transform ion cyclotron resonance mass spectrometer (FT-ICR MS) specially equipped to perform SID experiments [1].
• Similarly, the i.t. injection of DABK elicited thermal hyperalgesia in WT mice, but not in B(1)R KO mice [2].
• The B(1) receptor agonist, des-Arg(9)-Bradykinin (BK) (3.2 - 32.5 nmol), evoked dose-dependent increases in MAP and tachycardia during the first 10 min post-injection in STZ-diabetic rats only [3].

High impact information on 1-Des-arg-bradykinin

• Interestingly, the hemodynamic response to kinins was altered in transgenic mice, with des-Arg(9)-bradykinin inducing blood pressure increase when intravenously administered [4].
• 2 The intrapleural injection (i.pl.) of des-Arg(9)-bradykinin (des-Arg(9)-BK) (50 and 100 nmol per site), a selective B(1) receptor agonist, increased time-dependently the mononuclear and neutrophil cells influx in the pleural cavity of rats treated with STZ (65 mg kg(-1), i.p., 4 days earlier) [5].
• Bradykinin and des-Arg(9)-bradykinin metabolic pathways and kinetics of activation of human plasma [6].
• B(1) bradykinin receptor agonist (des-Arg(9)-bradykinin, 10(-10)-10(-8) mol/l) did not significantly affect vascular tone in control or beta-Gal gene-transduced canine basilar arteries without endothelium [7].
• Bolus injections of bradykinin (1-1000 pmol) but not des-Arg(9)-bradykinin (bradykinin B(1) receptor agonist) induced triphasic vascular responses: the initial sharp vasodilation followed by transient vasoconstriction and subsequent gradual vasodilation [8].

Chemical compound and disease context of 1-Des-arg-bradykinin

• The i.t. injection of the kinin B(1) receptor agonists, des-Arg(9)-bradykinin (DABK) or des-Arg(10)-kallidin (DAKD) also caused dose-related thermal hyperalgesia [2].

Biological context of 1-Des-arg-bradykinin

• These findings demonstrate that the activation of B1KR in VSMCs leads to the generation of second messengers that converge to activate MAPK and provide a rationale to investigate the mitogenic actions of dABK in vascular injury [9].
• In the present study, we provide evidence that des-Arg(9)-bradykinin (dABK) (10(-8) M), acting through B1KR, stimulates the phosphorylation of mitogen-activated protein kinase (MAPK) (p42(mapk) and p44(mapk)) [9].

Anatomical context of 1-Des-arg-bradykinin

• The most potent agonist for Chinese hamster ovary (CHO) cells stably expressing recombinant human bradykinin B(1) receptors were Des-Arg(9)-bradykinin (EC(50)=7.9 nM) and Des-Arg(10)-kallidin (EC(50)=8.6 nM), while the most potent agonist for CHO cells expressing human bradykinin B(2) receptors was bradykinin (EC(50)=2.0 nM) [10].
• The vasoconstrictive action on epicardial coronary arteries of des-Arg(9)-bradykinin in humans argues for a predominant action of B1-receptor stimulation at the level of smooth muscle cells [11].

Gene context of 1-Des-arg-bradykinin

• Activation of MAPK by dABK is mediated via a cholera toxin-sensitive pathway and appears to involve protein kinase C, Src kinase, and MAPK kinase [9].

References