Role of the B1 Bradykinin Receptor and gC1qR/p33 in Angioedema

Patients affected by angioedema (AE) are subject to asymmetric, nonerythematous, nonpruritic, localized, transient, episodic swelling of deeper layers or submucosal tissues of the skin, oropharyngolaryngeal tissue, and/or gastrointestinal wall. The nonapeptide bradykinin (BK) may be largely responsible for the vascular permeability seen in most AE. During AE attacks, activation of the serine proteases leads to the release of BK. Enzymes expressed on the endothelial cell membrane can metabolize BK, producing the agonist of the B1R, which can then be upregulated by proinflammatory stimuli, suggesting that the blockade of B1R and B2R, or gC1q/p33, may provide novel therapeutic targets.