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.