Renin–angiotensin system MCQs With Answer for B. Pharm students offers a focused, exam-oriented introduction to the physiology, biochemistry, pharmacology and clinical relevance of the renin–angiotensin–aldosterone system (RAAS). This concise, keyword-rich overview covers renin release mechanisms, angiotensinogen cleavage, ACE/ACE2 roles, AT1/AT2 receptor signalling, aldosterone effects, and therapeutic targets such as ACE inhibitors, ARBs and direct renin inhibitors. Ideal for pharmacy undergraduates preparing for exams or clinical rotations, these MCQs emphasize mechanisms, drug interactions, adverse effects and laboratory implications to build deeper conceptual understanding. Now let’s test your knowledge with 50 MCQs on this topic.
Q1. Which enzyme catalyzes the conversion of angiotensinogen to angiotensin I?
- Angiotensin-converting enzyme (ACE)
- Renin
- Angiotensinase
- ACE2
Correct Answer: Renin
Q2. Angiotensin II primarily exerts its vasoconstrictive effects via which receptor subtype?
- AT2 receptor
- Mas receptor
- AT1 receptor
- Beta-1 adrenergic receptor
Correct Answer: AT1 receptor
Q3. Which organ is the major source of angiotensinogen production?
- Kidney
- Liver
- Adrenal cortex
- Heart
Correct Answer: Liver
Q4. ACE inhibitors lower blood pressure chiefly by which mechanism?
- Blocking AT1 receptors
- Inhibiting renin release from juxtaglomerular cells
- Preventing conversion of angiotensin I to angiotensin II
- Stimulating aldosterone synthesis
Correct Answer: Preventing conversion of angiotensin I to angiotensin II
Q5. Which peptide is produced by ACE2 acting on angiotensin II and has vasodilatory effects?
- Angiotensin III
- Angiotensin IV
- Angiotensin (1–7)
- Bradykinin
Correct Answer: Angiotensin (1–7)
Q6. Direct renin inhibitors (e.g., aliskiren) act by which mechanism?
- Blocking AT1 receptors
- Inhibiting renin’s enzymatic activity on angiotensinogen
- Enhancing ACE activity
- Antagonizing aldosterone receptors
Correct Answer: Inhibiting renin’s enzymatic activity on angiotensinogen
Q7. Which effect is NOT typically associated with angiotensin II?
- Stimulating aldosterone release
- Increasing renal sodium reabsorption
- Inhibiting sympathetic neurotransmission
- Vasoconstriction
Correct Answer: Inhibiting sympathetic neurotransmission
Q8. Bradykinin accumulation due to ACE inhibition primarily contributes to which adverse effect?
- Hyperkalemia
- Dry cough
- Hypoglycemia
- Peripheral edema
Correct Answer: Dry cough
Q9. Aldosterone acts mainly on which part of the nephron to increase sodium reabsorption?
- Proximal tubule
- Loop of Henle
- Distal convoluted tubule and collecting duct
- Glomerulus
Correct Answer: Distal convoluted tubule and collecting duct
Q10. Elevated plasma renin activity with hypertension suggests which classification?
- Volume-dependent hypertension
- Low-renin hypertension
- Renin-dependent hypertension
- Pseudo-hypertension
Correct Answer: Renin-dependent hypertension
Q11. Which of the following is a common biochemical effect of chronic ACE inhibitor therapy?
- Hypokalemia
- Hyperkalemia
- Increased aldosterone secretion
- Enhanced angiotensin II levels
Correct Answer: Hyperkalemia
Q12. Which angiotensin metabolite can stimulate vasopressin release and has central nervous system actions?
- Angiotensin I
- Angiotensin II
- Angiotensin IV
- Angiotensin (1–7)
Correct Answer: Angiotensin II
Q13. Which receptor subtype is associated with antiproliferative and vasodilatory effects often opposing AT1?
- AT1 receptor
- AT2 receptor
- Mas receptor
- Beta-2 receptor
Correct Answer: AT2 receptor
Q14. Which laboratory test is most directly used to assess renin activity?
- Plasma aldosterone concentration
- Plasma renin activity (PRA)
- Serum ACE level
- Urine catecholamines
Correct Answer: Plasma renin activity (PRA)
Q15. Angiotensin III (Ang III) differs from angiotensin II primarily in that it:
- Has no biological activity
- Is generated by ACE from angiotensin I
- Can stimulate aldosterone release but is less potent vasoconstrictor
- Blocks AT1 receptors
Correct Answer: Can stimulate aldosterone release but is less potent vasoconstrictor
Q16. Which antihypertensive class directly blocks the AT1 receptor, reducing angiotensin II effects?
- ACE inhibitors
- Beta-blockers
- Angiotensin receptor blockers (ARBs)
- Calcium channel blockers
Correct Answer: Angiotensin receptor blockers (ARBs)
Q17. ACE is identical to which enzyme involved in bradykinin metabolism?
- Neutral endopeptidase (NEP)
- Kininase II
- Carboxypeptidase
- Monoamine oxidase
Correct Answer: Kininase II
Q18. A contraindication to ACE inhibitor therapy is:
- Pregnancy
- Type 2 diabetes mellitus without proteinuria
- Controlled asthma
- Mild hyperlipidemia
Correct Answer: Pregnancy
Q19. Which drug interaction increases the risk of hyperkalemia when combined with ACE inhibitors?
- Thiazide diuretics
- Loop diuretics
- Potassium-sparing diuretics (e.g., spironolactone)
- Beta-agonists
Correct Answer: Potassium-sparing diuretics (e.g., spironolactone)
Q20. What is the main physiological trigger for renin release from juxtaglomerular cells?
- Increased renal perfusion pressure
- Decreased renal perfusion pressure
- Elevated atrial natriuretic peptide (ANP)
- High sodium concentration at the macula densa
Correct Answer: Decreased renal perfusion pressure
Q21. ACE inhibitors may be renoprotective in diabetic nephropathy by:
- Increasing intraglomerular pressure
- Reducing efferent arteriolar constriction and glomerular hypertension
- Stimulating aldosterone release
- Enhancing sodium reabsorption in the proximal tubule
Correct Answer: Reducing efferent arteriolar constriction and glomerular hypertension
Q22. Which peptide fragment is generated from angiotensin II by aminopeptidase A?
- Angiotensin I
- Angiotensin III
- Angiotensin (1–7)
- Angiotensinogen
Correct Answer: Angiotensin III
Q23. Which adverse effect is more specific to ARBs compared to ACE inhibitors?
- Dry cough
- Angioedema
- Hyperkalemia
- Hypotension
Correct Answer: Hyperkalemia
Q24. In heart failure, RAAS activation contributes to progression by:
- Reducing preload and afterload
- Promoting vasodilation and diuresis
- Causing sodium retention, vasoconstriction and remodeling
- Inhibiting sympathetic tone
Correct Answer: Causing sodium retention, vasoconstriction and remodeling
Q25. Which statement about ACE2 is correct?
- ACE2 increases angiotensin II levels
- ACE2 converts angiotensin I directly to angiotensin II
- ACE2 converts angiotensin II to angiotensin (1–7)
- ACE2 is inhibited by ACE inhibitors
Correct Answer: ACE2 converts angiotensin II to angiotensin (1–7)
Q26. Which of the following is a direct downstream genomic effect of aldosterone in collecting duct cells?
- Decrease in ENaC expression
- Increase in Na+/K+ ATPase and ENaC expression
- Immediate vasodilation
- Inhibition of K+ secretion
Correct Answer: Increase in Na+/K+ ATPase and ENaC expression
Q27. Which enzyme deficiency would most directly decrease angiotensin II formation?
- Renin deficiency
- Thromboxane synthase deficiency
- Cyclooxygenase deficiency
- Renin receptor deficiency
Correct Answer: Renin deficiency
Q28. Which clinical condition is associated with low-renin hypertension?
- Renovascular hypertension
- Primary aldosteronism
- Renin-secreting tumor
- Dehydration-induced hypotension
Correct Answer: Primary aldosteronism
Q29. Which pharmacological effect distinguishes ARBs from ACE inhibitors?
- ARBs block bradykinin breakdown leading to cough
- ARBs directly antagonize AT1 receptors without increasing bradykinin
- ARBs inhibit renin enzymatic activity
- ARBs increase ACE activity
Correct Answer: ARBs directly antagonize AT1 receptors without increasing bradykinin
Q30. Which test pairing is useful for screening primary aldosteronism?
- Plasma renin activity low, plasma aldosterone high (elevated aldosterone-renin ratio)
- High PRA and low aldosterone
- Normal PRA and low aldosterone
- Urine cortisol low
Correct Answer: Plasma renin activity low, plasma aldosterone high (elevated aldosterone-renin ratio)
Q31. Which of the following peptides is least likely to be increased by ACE inhibition?
- Bradykinin
- Angiotensin I
- Angiotensin II
- Angiotensin (1–7)
Correct Answer: Angiotensin II
Q32. Which molecule acts as a prorenin receptor modulating local RAAS activity?
- AT1 receptor
- Renin receptor (PRR)
- ACE2 receptor
- Mas receptor
Correct Answer: Renin receptor (PRR)
Q33. Which is a mechanism by which angiotensin II promotes cardiac remodeling?
- Decreasing collagen synthesis
- Inhibiting fibroblast proliferation
- Stimulating hypertrophy and fibrosis via AT1 receptors
- Blocking TGF-beta signaling
Correct Answer: Stimulating hypertrophy and fibrosis via AT1 receptors
Q34. Which of the following is TRUE about angiotensin IV?
- Acts via AT1 receptor to increase blood pressure
- Has no known receptors
- May modulate cognitive function via IRAP (insulin-regulated aminopeptidase)
- Is the primary substrate for ACE2
Correct Answer: May modulate cognitive function via IRAP (insulin-regulated aminopeptidase)
Q35. When starting ACE inhibitor therapy, which parameter should be monitored closely within the first week?
- Liver enzymes
- Serum potassium and serum creatinine
- Fasting blood glucose
- Thyroid function tests
Correct Answer: Serum potassium and serum creatinine
Q36. Which physiologic signal from the macula densa increases renin secretion?
- High distal tubular NaCl concentration
- Low distal tubular NaCl concentration
- High blood pressure
- Increased atrial stretch
Correct Answer: Low distal tubular NaCl concentration
Q37. Which class of antihypertensive drugs can blunt renin release by inhibiting sympathetic beta-1 stimulation of juxtaglomerular cells?
- Calcium channel blockers
- Beta-blockers
- ACE inhibitors
- Thiazide diuretics
Correct Answer: Beta-blockers
Q38. In a patient on ACE inhibitors who develops angioedema, the appropriate immediate step is:
- Continue ACE inhibitor and observe
- Discontinue ACE inhibitor and avoid ARBs due to cross-reactivity risk
- Switch to an ARB without concern
- Increase ACE inhibitor dose
Correct Answer: Discontinue ACE inhibitor and avoid ARBs due to cross-reactivity risk
Q39. Which signalling pathway is commonly activated by AT1 receptor stimulation?
- cAMP-PKA pathway exclusively
- Gq/PLC-IP3/DAG pathway leading to increased intracellular calcium
- Inhibition of phospholipase C
- Activation of tyrosine kinase receptor pathways only
Correct Answer: Gq/PLC-IP3/DAG pathway leading to increased intracellular calcium
Q40. Which condition increases circulating angiotensinogen levels and may worsen hypertension?
- Hypothyroidism
- Estrogen therapy or pregnancy
- Adrenal insufficiency
- Decreased hepatic synthesis
Correct Answer: Estrogen therapy or pregnancy
Q41. Which statement is correct regarding ACE inhibitors and pregnancy?
- ACE inhibitors are safe in the first trimester
- ACE inhibitors are contraindicated during pregnancy due to fetal renal toxicity
- ACE inhibitors prevent congenital malformations
- ACE inhibitors increase placental perfusion and are recommended
Correct Answer: ACE inhibitors are contraindicated during pregnancy due to fetal renal toxicity
Q42. Which factor does NOT stimulate aldosterone secretion?
- Angiotensin II
- Hyperkalemia
- ACTH (adrenocorticotropic hormone) transiently
- Hypokalemia
Correct Answer: Hypokalemia
Q43. Which of the following best explains the combined use of ACE inhibitor and ARB in clinical practice?
- Routine combination improves outcomes universally
- Combination increases bradykinin and eliminates ARB side effects
- Combination may increase adverse effects (hyperkalemia, renal dysfunction) and is generally not recommended
- Combination prevents ACE inhibitor-induced cough
Correct Answer: Combination may increase adverse effects (hyperkalemia, renal dysfunction) and is generally not recommended
Q44. Which molecular change occurs when angiotensin II binds AT1 receptors on vascular smooth muscle?
- Decrease in intracellular calcium
- Activation of myosin light chain kinase leading to contraction
- Inhibition of phospholipase C
- Increased cAMP leading to relaxation
Correct Answer: Activation of myosin light chain kinase leading to contraction
Q45. Which drug is a prodrug that must be converted to its active form by hepatic esterases and is an ACE inhibitor?
- Lisinopril
- Captopril
- Enalapril
- Losartan
Correct Answer: Enalapril
Q46. Which of the following best describes the effect of RAAS blockade on proteinuria?
- RAAS blockade typically increases proteinuria
- RAAS blockade reduces intraglomerular pressure and decreases proteinuria
- RAAS blockade has no effect on proteinuria
- RAAS blockade directly increases glomerular basement membrane permeability
Correct Answer: RAAS blockade reduces intraglomerular pressure and decreases proteinuria
Q47. Which is the correct sequence of peptides in the classical RAAS cascade starting from angiotensinogen?
- Angiotensinogen → Angiotensin II → Angiotensin I → Aldosterone
- Angiotensinogen → Angiotensin I → Angiotensin II → Aldosterone
- Angiotensinogen → Aldosterone → Angiotensin I → Angiotensin II
- Angiotensinogen → Renin → ACE → Aldosterone
Correct Answer: Angiotensinogen → Angiotensin I → Angiotensin II → Aldosterone
Q48. Which pharmacokinetic property is important for ACE inhibitors to achieve once-daily dosing and tissue penetration?
- Very short half-life less than 1 hour
- High oral bioavailability and suitable half-life
- No hepatic metabolism required
- Complete renal excretion without protein binding
Correct Answer: High oral bioavailability and suitable half-life
Q49. Which signaling molecule is often upregulated by angiotensin II and contributes to fibrosis?
- cGMP
- TGF-β (transforming growth factor-beta)
- Atrial natriuretic peptide (ANP)
Correct Answer: TGF-β (transforming growth factor-beta)
Q50. Which clinical scenario most likely warrants measurement of plasma renin activity and aldosterone levels?
- Young patient with resistant hypertension and hypokalemia
- Single episode of uncomplicated mild hypertension
- Controlled hypertension on monotherapy
- Hyperthyroidism without hypertension
Correct Answer: Young patient with resistant hypertension and hypokalemia
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