Pathology · Inflammation (Acute, Chronic, Granulomatous, Mediators)

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
Correct answer: 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.

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