Bradykinin MCQs With Answer provide B.Pharm students a targeted review of the kinin–kallikrein system. Bradykinin is a key inflammatory mediator central to vasodilation, increased vascular permeability, pain signalling, and pharmacological interactions such as ACE inhibitor–induced cough and angioedema. This set of focused MCQs with answers deepens understanding of synthesis (kallikrein, HMWK/LMWK), receptor pharmacology (B1 vs B2), intracellular signalling (PLC, NO, prostacyclin), metabolic pathways (ACE, neprilysin, carboxypeptidases) and clinical relevance (hereditary angioedema, icatibant, ecallantide). Questions emphasize mechanism, drug interactions, therapeutic targets and diagnostic considerations to prepare you for exams and clinical pharmacy practice.
Now let’s test your knowledge with 30 MCQs on this topic.
Q1. Which statement best describes the enzymatic formation of bradykinin?
- Generated from high molecular weight kininogen by kallikrein
- Cleaved directly from angiotensin I by ACE
- Synthesized as a peptide hormone in the adrenal medulla
- Formed from prekallikrein by angiotensinogen
Correct Answer: Generated from high molecular weight kininogen by kallikrein
Q2. Kallidin (Lys‑bradykinin) differs from bradykinin because it is produced from which precursor?
- High molecular weight kininogen (HMWK)
- Low molecular weight kininogen (LMWK)
- Preprobradykinin in endothelial cells
- Angiotensinogen in the liver
Correct Answer: Low molecular weight kininogen (LMWK)
Q3. Which bradykinin receptor is constitutively expressed and mediates most normal physiological effects?
- B2 receptor, constitutively expressed
- B1 receptor, constitutively expressed
- B3 receptor, expressed on leukocytes
- β‑adrenergic receptor, constitutively expressed
Correct Answer: B2 receptor, constitutively expressed
Q4. The B1 bradykinin receptor is best characterized by which feature?
- Inducible expression and preferential activation by des‑Arg9‑bradykinin
- Constitutive expression and binding of native bradykinin only
- Activation by angiotensin II during stress
- Direct coupling to β‑adrenergic signalling pathways
Correct Answer: Inducible expression and preferential activation by des‑Arg9‑bradykinin
Q5. Which enzyme is also called kininase II and is a major route for bradykinin degradation?
- Angiotensin‑converting enzyme (ACE)
- Neprilysin (neutral endopeptidase)
- Carboxypeptidase N
- Aminopeptidase P
Correct Answer: Angiotensin‑converting enzyme (ACE)
Q6. The persistent dry cough seen with ACE inhibitor therapy is primarily due to which mechanism?
- Accumulation of bradykinin in the respiratory tract due to reduced degradation by ACE
- Activation of β2 receptors in bronchial smooth muscle
- Direct histamine release from mast cells by ACE inhibitors
- Increased angiotensin II stimulating sensory nerves
Correct Answer: Accumulation of bradykinin in the respiratory tract due to reduced degradation by ACE
Q7. Bradykinin induces vasodilation primarily through which endothelial mediators?
- Stimulation of nitric oxide (NO) and prostacyclin release
- Direct blockade of adrenergic receptors on smooth muscle
- Activation of endothelin synthesis
- Inhibition of cyclooxygenase and thromboxane
Correct Answer: Stimulation of nitric oxide (NO) and prostacyclin release
Q8. Which vascular effect of bradykinin explains its role in inflammatory edema?
- Increases vascular permeability leading to plasma extravasation and edema
- Causes vasoconstriction and reduced tissue perfusion
- Stimulates lymphatic drainage to reduce swelling
- Enhances albumin synthesis to restore oncotic pressure
Correct Answer: Increases vascular permeability leading to plasma extravasation and edema
Q9. Which drug is a selective B2 receptor antagonist used to treat acute bradykinin‑mediated angioedema?
- Icatibant (a selective B2 receptor antagonist)
- Losartan (an angiotensin receptor blocker)
- Diphenhydramine (an H1 antihistamine)
- Prednisone (a glucocorticoid)
Correct Answer: Icatibant (a selective B2 receptor antagonist)
Q10. Ecallantide exerts its therapeutic effect in hereditary angioedema by which mechanism?
- Inhibiting plasma kallikrein to reduce bradykinin generation
- Blocking histamine H1 receptors to reduce swelling
- Inhibiting ACE to increase angiotensin II
- Stabilizing mast cell membranes to prevent degranulation
Correct Answer: Inhibiting plasma kallikrein to reduce bradykinin generation
Q11. Hereditary angioedema (HAE) type I and II are most commonly caused by deficiency or dysfunction of which protein?
- C1 esterase inhibitor (C1‑INH), leading to unchecked kallikrein activity and bradykinin excess
- ACE, leading to increased bradykinin degradation
- Factor VIII, leading to bleeding and swelling
- Histidine decarboxylase, leading to excess histamine
Correct Answer: C1 esterase inhibitor (C1‑INH), leading to unchecked kallikrein activity and bradykinin excess
Q12. The discovery of bradykinin potentiating peptides from Bothrops jararaca venom contributed to development of which drug class?
- ACE inhibitors
- Beta‑blockers
- Calcium channel blockers
- Prostaglandin analogues
Correct Answer: ACE inhibitors
Q13. Which enzyme removes the C‑terminal arginine from bradykinin to generate des‑Arg9‑bradykinin?
- Carboxypeptidase N (kininase I)
- Neprilysin (neutral endopeptidase)
- Angiotensin‑converting enzyme (ACE)
- Aminopeptidase P
Correct Answer: Carboxypeptidase N (kininase I)
Q14. Activation of which bradykinin receptor subtype is most implicated in acute nociception and pain sensitization?
- B2 receptor, sensitizing peripheral nociceptors
- B1 receptor, mediating acute nociception only
- B3 receptor, located in dorsal horn exclusively
- μ‑opioid receptor, via indirect modulation
Correct Answer: B2 receptor, sensitizing peripheral nociceptors
Q15. Bradykinin B2 receptor primarily signals via which G‑protein pathway?
- Gq protein leading to PLC activation, IP3 production and increased intracellular Ca2+
- Gs protein increasing cAMP and PKA activation
- Gi protein decreasing cAMP only
- G12/13 exclusively causing Rho activation
Correct Answer: Gq protein leading to PLC activation, IP3 production and increased intracellular Ca2+
Q16. Which statement about bradykinin’s plasma half‑life is correct?
- Very short due to rapid enzymatic degradation by ACE and other peptidases
- Long and stores in platelets for release on demand
- Stable in plasma because it binds albumin tightly
- Not degraded in plasma; only cleared by the kidney
Correct Answer: Very short due to rapid enzymatic degradation by ACE and other peptidases
Q17. Besides ACE inhibitors, which class of drugs can increase bradykinin levels by inhibiting neprilysin?
- Neprilysin inhibitors such as sacubitril
- Beta‑blockers such as propranolol
- Calcium channel blockers such as amlodipine
- Statins such as atorvastatin
Correct Answer: Neprilysin inhibitors such as sacubitril
Q18. In hereditary angioedema, which complement laboratory finding is typically decreased?
- Complement C4 and C1‑INH levels/activity are decreased
- C3 levels are markedly elevated
- C‑reactive protein is undetectable
- Antistreptolysin O titers are increased
Correct Answer: Complement C4 and C1‑INH levels/activity are decreased
Q19. Bradykinin increases endothelial permeability through which cellular mechanism?
- Elevation of endothelial intracellular Ca2+ causing cytoskeletal contraction and intercellular gap formation
- Stabilization of endothelial tight junctions to reduce leakage
- Induction of endothelial apoptosis to remove barriers
- Direct cleavage of basement membrane proteins to allow plasma flow
Correct Answer: Elevation of endothelial intracellular Ca2+ causing cytoskeletal contraction and intercellular gap formation
Q20. Which metabolite preferentially activates the inducible B1 receptor?
- Des‑Arg9‑bradykinin
- Lys‑bradykinin (kallidin)
- Angiotensin II
- Bradykinin‑1–7 fragment
Correct Answer: Des‑Arg9‑bradykinin
Q21. The net effect of bradykinin on systemic blood pressure is usually:
- Hypotension due to vasodilation and natriuretic effects
- Hypertension due to strong vasoconstriction
- No change because effects are limited to microcirculation
- Transient hypertension via increased heart rate
Correct Answer: Hypotension due to vasodilation and natriuretic effects
Q22. Bradykinin contributes to inflammation by which of the following actions?
- Promoting release of other mediators and enhancing leukocyte recruitment
- Directly lysing bacteria as an antimicrobial peptide
- Inhibiting prostaglandin synthesis to reduce swelling
- Blocking chemokine receptors on neutrophils
Correct Answer: Promoting release of other mediators and enhancing leukocyte recruitment
Q23. The term “kininase I” historically refers to which enzyme activity?
- Carboxypeptidase N removing the terminal arginine from bradykinin
- Angiotensin‑converting enzyme (ACE) cleavage of bradykinin
- Neprilysin hydrolysis producing inactive fragments
- Aminopeptidase P cleaving the N‑terminus of bradykinin
Correct Answer: Carboxypeptidase N removing the terminal arginine from bradykinin
Q24. Bradykinin can provoke respiratory symptoms; which effect is commonly observed?
- Bronchoconstriction and cough via sensory nerve activation
- Bronchodilation and reduced airway resistance
- Suppression of mucus secretion in airways
- Direct inhibition of pulmonary surfactant
Correct Answer: Bronchoconstriction and cough via sensory nerve activation
Q25. Which plasma enzyme contributes significantly to bradykinin degradation and varies among individuals?
- Aminopeptidase P
- Renin
- Thromboxane synthase
- Glutathione peroxidase
Correct Answer: Aminopeptidase P
Q26. The vasodilator effects of bradykinin are abolished when which of the following is removed?
- Endothelium, since bradykinin requires endothelial NO/prostacyclin release
- Smooth muscle cells, because bradykinin acts intracellularly there
- Plasma proteins, as bradykinin is protein‑bound
- Nerve supply, since bradykinin works through neuronal reflexes
Correct Answer: Endothelium, since bradykinin requires endothelial NO/prostacyclin release
Q27. Which plasma protein serves as the direct precursor for bradykinin peptides?
- High molecular weight kininogen (HMWK)
- Low density lipoprotein (LDL)
- Albumin
- Fibrinogen
Correct Answer: High molecular weight kininogen (HMWK)
Q28. Combining an ACE inhibitor with a neprilysin inhibitor increases risk of angioedema because:
- Both inhibit bradykinin degradation and cause bradykinin accumulation
- ACE inhibitors stimulate bradykinin synthesis while neprilysin inhibitors block its receptor
- Neprilysin activation increases angiotensin II leading to swelling
- The combination causes immunosuppression leading to mast cell degranulation
Correct Answer: Both inhibit bradykinin degradation and cause bradykinin accumulation
Q29. In the contact activation pathway, which activated factor converts prekallikrein to kallikrein?
- Activated factor XII (XIIa)
- Factor Xa directly
- Plasminogen activator
- Thrombin (factor IIa)
Correct Answer: Activated factor XII (XIIa)
Q30. The most direct and specific acute therapy for hereditary angioedema due to C1‑INH deficiency is:
- C1 esterase inhibitor concentrate replacement
- High‑dose intravenous corticosteroids
- Oral antihistamines alone
- Beta‑agonist inhalation therapy
Correct Answer: C1 esterase inhibitor concentrate replacement
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