缓激肽B1受体抗体

缓激肽B1受体抗体 Background: Kinins are important biologically active peptides that mediate cardiovascular homeostasis, inflammation and nociception. Bradykinin, the major effector peptide of the kallikrein-kinin system, is regulated by angiotensin-converting enzyme (ACE), which degrades the peptide. Bradykinin normally exerts its effects through the activation of two seven transmembrane G-protein coupled receptors, named B1 and B2. The B2 receptor is constitutively expressed and preferentially binds full length bradykinin. Deletion of the B2 receptor leads to salt-sensitive hypertension and altered nociception in mice. The B1 receptor binds to derivatives of bradykinin and kallidin, which are produced by carboxypeptidase action to generate the products des-Arg9-bradykinin and des-Arg10-kallidin, respectively. The expression of the B1 receptor is inducible by inflammatory mediators, such as bacterial lipopolysaccharide (LPS) and cytokines. The B1 and B2 receptors represent potential therapeutic targets for treatment of inflammatory disorders and cardiovascular diseases. Also known as: B1 bradykinin receptor; B1BKR; B1R; BDKR B1; BDKRB 1; BDKRB1; BK 1 receptor; BK-1 receptor; bradykinin B1 R; BKB1R; BKR 1; BKR1; BKRB1_HUMAN; BRADY B1; BRADYB1; Bradykinin B1 receptor; Bradykinin receptor 1; bradykinin B1R; Bradykinin receptor B1缓激肽B1受体抗体