Lys-Bradykinin

Lys-Bradykinin. B2 Bradykinin Receptor Ligand.
Kinins are small peptides rapidly produced following tissue injury that serve as important modulators of inflammation and pain. In the periphery, the actions of kinins include vasodilatation, increased vascular permeability, stimulation of immune cells, and induction of pain. Kinins in the central nervous system (CNS) appear to initiate a similar cascade of events leading to neural tissue damage as well as long lasting disturbances affecting blood-brain barrier function.
Kinins such as Bradykinin (BK), Lys-BK, desArg\\^9\\-BK, and Lys-desArg\\^9\\-BK exert their action via two distinct G protein-coupled receptors (GPCR): the B\\_1\\ Bradykinin receptor (BKRB1) and the B\\_2\\ Bradykinin receptor (BKRB2).
Activation of BKRB2 liberates mediators of vascular tone, fibrinolysis, and pain. BKRB2, which mediates most of the physiological effects of kinins, as well as BKRB1, represent potential therapeutic targets for treatment of inflammatory disorders and cardiovascular diseases.
Expression of BKRB1 is inducible upon various types of tissue injury and by inflammatory mediators such as bacterial lipopolysaccharide (LPS) and cytokines. A low level of expression of BKRB1 in the CNS of rodent and primates was recently demonstrated.
BKRB2 is constitutively and widely expressed throughout the CNS and peripheral nervous system and on various cell types including endothelial cells, nerve fibers, leukocytes, and mast cells.

Lys-Bradykinin is an endogenous nonspecific agonist for BKRB1and BKRB2, with some specificity towards the BKRB2. Activation of Bradykinin receptors with Lys-Bradykinin may induce intracellular Ca²⁺ elevation. 100 nM Lys-Bradykinin induced Ca²⁺ transients in rat aortic endothelium cells (RAEC) (see figure here and review in reference #8).
G-Protein Coupled Receptor Ligands; Bradykinin Receptor Ligands

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