Modulations of the kallikrein-kinin system lead to changes in the endothelial barrier

Introduction Bradykinin-mediated angioedema arises from changes in the bradykinin metabolism. An increase in bradykinin concentration causes enhanced vascular permeability. Hereditary angioedema (HAE) results from a disorder of bradykinin synthesis (deficient or defective C1-INH). Drugs such as ACE inhibitors can also cause angioedema by blocking degradation. This study aims the first establishment of an in vitro kallikrein-kinin system (KKS) to explore the effects of changes in bradykinin metabolism on endothelial barrier function.