Bradykinin is a key mediator of the pain, vasodilation, and increased vascular permeability seen in acute inflammation. It is generated from kininogen by the enzyme:

• A Kallikrein (plasma and tissue) ✓
• B Plasmin
• C Thrombin
• D Factor Xa

Explanation

Bradykinin (a nonapeptide) is cleaved from high-molecular-weight kininogen (HMWK) by plasma kallikrein and from low-molecular-weight kininogen by tissue kallikrein. The kallikrein-kinin system is activated when Hageman factor (Factor XII) binds to exposed subendothelial collagen, activating kallikrein from prekallikrein. Bradykinin causes vasodilation, increased vascular permeability (by contracting endothelial cells), smooth muscle contraction, and pain — effects mediated via B2 receptors. ACE (kininase II) rapidly degrades bradykinin; ACE inhibitor-associated angioedema results from bradykinin accumulation.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.