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- Bathon, J. M. and Proud, D. (1991) Annu. Rev. Pharmacol. Toxicol. 31, 129.
- Alomone Labs Bradykinin induces store-operated Ca2+ release in RAEC cells.Cells were loaded with Fluo-3 AM. Intracellular Ca2+ fluctuations were measured in the presence of EGTA and increasing Bradykinin (#GPB-200) concentrations. The fluorescence is plotted against Bradykinin concentrations (ED50 = 93 ng/ml).
- Bhoola, K.D. et al. (1992) Pharmacol. Rev. 44, 1.
- Brechter, A.B. and Lerner, U. H. (2007) Arthritis Rheum. 56, 910.
- Joseph, K. and Kaplan, A. P. 2005 Adv. Immunol. 86, 159.
- Marceau, F. et al. (1983) Gen. Pharmacol. 14, 209.
- Shin, Y. H. et al. (1996) Immunopharmacology 33, 369.
- Walker, K. et al. (1995) Neurochem. Int. 26, 1.
Bradykinin is a potent effector peptide that binds the bradykinin receptors B2. Bradykinin reduces blood pressure and increases vascular permeability by inducing smooth muscle relaxation and blood vessel dilation1.
Bradykinin is one the most potent known factors inducing pain substances that acts on afferent sensory neurons Bradykinin stimulates the synthesis of prostaglandins2 and is a major contributor to the innate inflammatory response3. Injection of Bradykinin into the skin produces all the inflammation basic signs4. Bradykinin has been implicated also in various shock syndromes5. Application of Bradykinin to the central nervous system appears to initiate events leading to neural tissue damage as well as long lasting disturbances affecting blood-brain barrier function6.
Bradykinin (#GPB-200) is a highly pure, synthetic, and biologically active protein.
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