Which statement about bradykinin in acute inflammation is correct?
- A It acts mainly through B1 receptors on endothelium under basal conditions
- B It produces vasodilation, increased vascular permeability, and is a mediator of pain
- C It is generated directly by activation of the complement cascade at C3 level
- D It is rapidly degraded by angiotensin-converting enzyme, hence ACE inhibitors prolong its action ✓
Explanation
Bradykinin is generated from high-molecular-weight kininogen by kallikrein, downstream of activated Hageman factor (factor XII). It causes vasodilation, increases venular permeability, and is a potent mediator of pain. It is inactivated by kininases, chiefly kininase II, which is identical to angiotensin-converting enzyme; this explains why ACE inhibitors can precipitate angioedema. Option A is wrong because bradykinin acts constitutively through B2 receptors; B1 receptors are inducible.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.