Bradykinin Metabolism and Drug-Induced Angioedema

Bradykinin (BK) metabolism and its receptors play a central role in drug-induced angioedema (AE) without urticaria through increased vascular permeability. Many cardiovascular and diabetic drugs may cause BK-mediated AE. Angiotensin-converting enzyme inhibitors (ACEIs) and neprilysin inhibitors impair BK catabolism. Dipeptidyl peptidase-IV (DPP-IV) inhibitors reduce the breakdown of BK and substance P (SP). Moreover, angiotensin receptor blockers, thrombolytic agents, and statins may also induce BK-mediated AE. Understanding pathophysiological mechanisms is crucial for preventing and treating drug-induced AE.

Automated summary

Bradykinin metabolism and its receptors are crucial in drug-induced angioedema without urticaria due to increased vascular permeability. Many cardiovascular and diabetic drugs can cause BK-mediated AE. Inhibition of angiotensin-converting enzyme and neprilysin impair BK catabolism. Dipeptidyl peptidase-IV inhibitors reduce the breakdown of BK and substance P. Additionally, angiotensin receptor blockers, thrombolytic agents, and statins may also induce BK-mediated AE. Understanding the pathophysiological mechanisms is essential for preventing and treating drug-induced AE.